ACROLEIN
ACROLEIN
CASRN: 107-02-8
http://toxnet.nlm.nih.gov/cgi-bin/sis/search/r?./temp/~AAAXUaWSc:@DOCNO+@term+177
Human Health Effects:
Toxicity Summary:
Acrolein is very toxic to aquatic organisms.
Acute EC50 and LC50 values for bacteria, algae, crustacea, and fish are between
0.02 and 2.5 mg/liter, bacteria being the most sensitive species. ... In animals
and humans the reactivity of acrolein effectively confines the substance to the
site of exposure, and pathological findings are also limited to these sites. ...
Acrolein reacts directly with protein and non-protein sulfhydryl groups and with
primary and secondary amines. It may also be metabolized to mercapturic acids,
acrylic acide, glycidaldehyde or glyceraldehyde. Evidence for the last three
metabolites has only been obtained in vitro. Acrolein is a cytotoxic agent. In
vitro cytotoxicity has been observed as low as 0.1 mg/liter. The substance is
highly toxic to experimental animals and humans following a single exposure via
different routes. The vapor is irritating to the eyes and respiratory tract.
Liquid acrolein is a corrosive substance. ... At higher single exposure levels,
degeneration of the respiratory epithelium, inflammatory sequelae, and
perturbation of respiratory function develop. ... In general, body weight gain
reduction, decrement of pulmonary function, and pathological changes in nose,
upper airways, and lungs have been documented in most species exposed to
concentrations of 1.6 mg/cu m or more for 8 hr/day. Pathological changes include
inflammation, metaplasia, and hyperplasia of the respiratory tract. Significant
mortality has been observed following repeated exposures to acrolein vapor at
concentrations above 9.7 mg/ cu m. In experimental animals acrolein has been
shown to deplete tissue glutathione and in in vitro studies, to inhibit enzymes
by reacting with sulfhydryl groups at active sites. There is limited evidence
that acrolein can depress pulmonary host defenses in mice and rats. Acrolein can
induce teratogenic and embryotoxic effects if administered directly into the
amnion. ... Acrolein has been shown to interact with nucleic acids in vitro and
to inhibit their synthesis both in vitro and in vivo. Without activation it
induced gene mutations in bacteria and fungi and caused sister chromatid
exchanges in mammalian cells. ... The threshold levels of acrolein causing
irritation and health effects are 0.7 mg/ cu m for odor perception, 0.13 mg/cu m
for eye irritation, 0.3 mg/ cu m for nasal irritation and eye blinking, and 0.7
mg/ cu m for decreased respiratory rate. ... In view of the high toxicity of
acrolein to aquatic organisms, the substance presents a risk to aquatic life at
or near sites of industrial discharges, spills and biocidal use.
Evidence for Carcinogenicity:
CLASSIFICATION: C; possible human carcinogen.
BASIS FOR CLASSIFICATION: Classification is based on increased incidence of
adrenal cortical adenomas to female rats and carcinogenic potential of an
acrolein metabolite. Acrolein is mutagenic in bacteria and is structurally
related to probable or known human carcinogens. HUMAN CARCINOGENICITY DATA:
None. ANIMAL CARCINOGENICITY DATA: Limited.
Evaluation: There is inadequate evidence in
humans for the carcinogenicity of acrolein. There is inadequate evidence in
experimental animals for the carcinogenicity of acrolein. Overall evaluation:
Acrolein is not classifiable as to its carcinogenicity to humans (Group 3).
Human Toxicity Excerpts:
IT IRRITATES SKIN, MUCOUS MEMBRANES. VAPORS
CAUSE LACRIMATION. WEAK SENSITIZER; INHALATION MAY CAUSE ASTHMATIC REACTION.
... /INHALATION CAUSES/ IRRITATION OF NOSE
& THROAT, TIGHTNESS OF CHEST, & SHORTNESS OF BREATH, NAUSEA &
VOMITING. BRONCHOPULMONARY EFFECT IS VERY SEVERE; EVEN IF VICTIM RECOVERS FROM
ACUTE EXPOSURE, THERE WILL BE PERMANENT RADIOLOGICAL & FUNCTIONAL DAMAGE.
Exposure to 1 ppm (2.3 mg/cu m) acrolein vapor
in air causes lacrimation & marked eye, nose & throat irritation within
a period of 5 min. Acrolein is a severe pulmonary irritant & powerful
lachrymogen at a concn of 3 ppm (7 mg/cu m) & greatly irritates the
conjunctiva & mucous membranes of upper resp tract. At higher concn it ...
causes injury to lung; Resp insufficiency may persist for at least 18 mo after
exposure. A 10 min exposure to 350 mg/cu m was lethal.
... Skin contact with liquid acrolein /has
been described/ as causing irritation, erythema, & edema, & a splash in
the eye as causing blepharoconjunctivitis, lid edema, fibrinous or purulent
discharge, & corneal injury, which ... may be deep & long-lasting. ...
Severe damage is possible as from alkali burns ... .
INHALATION OF AIR CONTAINING 10 PPM ACROLEIN
MAY BE FATAL IN A FEW MIN.
Acrolein ... is a well-established respiratory
irritant.
Intense lacrimation & nasal irritation
ordinarily give adequate warning of inhalation, but exposed patients should be
observed for 24 hr for a slowly developing pulmonary edema.
Acrolein increases airway resistance and tidal
volume and decreases respiratory frequency.
Aldehydes increase airflow at concentrations
below those that decrease respiratory frequency. /Aldehydes/
The ability of the highly reactive aldehyde
acrolein to affect growth, membrane integrity, differentiation, and thiol status
and to cause DNA damage has been studied at serum and thiol free conditions
using cultured human bronchial epithelial cells. Acrolein markedly decreases
colony survival at 3 uM whereas about 10 fold higher concentrations are required
to increase membrane permeability, measured as uptake of trypan blue dye.
Acrolein at uM concentrations also causes epithelial cells to undergo squamous
differentiation as indicated by decreased clonal growth rate, dose dependent
increased formation of cross linked envelopes, and increased cell planar surface
area. Acrolein causes a marked and dose dependent cellular depletion of total
and specific free low molecular weight thiols as well as protein thiols.
Exposure to acrolein did not cause oxidation of glutathione indicating that
thiol depletion occurred by direct conjugation of reduced glutathione to
acrolein without concomitant generation of active oxygen species. Furthermore,
acrolein is genotoxic and causes both DNA single strand breaks and DNA protein
cross-links in human bronchial epithelial cells. The results indicate that
acrolein causes several cytopathic effects that relate to multistage
carcinogenesis in the human bronchial epithelium.
... The purpose of this study was to: (a)
compare the relative abilities of phosphoramide mustard and acrolein to induce
cytogenetic damage and cytotoxicity in cultured human lymphocytes; (b) assess
the efficacy of 2-mercaptoethanesulfonic acid to attenuate the cytogenetic
damage and cytotoxicity induced by cyclophosphamide, acrolein, phosphoramide
mustard, and diethyl-4'-hydroperoxycyclophosphamide, an activated acrolein
generating compound; and (c) determine if concanavalin A stimulated
T-lymphocytes, which differentiate into suppressor cells upon lectin activation,
exhibit any heightened cytogenetic sensitivity compared to a variety of cultured
mammalian cells during exposure to phosphoramide mustard or acrolein as reported
by other investigators. Purified mononuclear leukocytes were stimulated with
concanavalin A and exposed to cyclophosphamide (0.5-2.0 mM) without and
exogenous activation system, acrolein (0.001-40.0 uM), phosphoramide mustard
(0.0014-27.1 uM), or diethyl-4'-hydroperoxycyclophosphamide (0.1-100.0 uM) in
the presence or absence of 2-mercaptoethansulfonic acid (1, 5, or 10 mM). All
four compounds induced significant concentration related increases in the sister
chromatid exchange frequency, but only phosphoramide mustard was clastogenic. On
an induced sister chromatid exchange/uM basis, phosphoramide mustard was 130 and
193 times more potent than were diethyl-4'-hydroperoxycyclophosphamide and
acrolein respectively. 2-Mercaptoethanesulfonic acid protected against the
cytogenetic damage and cytotoxicity induced by the four compounds, but it was
particularly effective against acrolein and
diethyl-4'-hydroperoxycyclophosphamide by abolishing sister chromatid exchange
induction completely. Sister chromatid exchanges and chromosome aberrations
differed considerably in their induction kinetics in lymphocytes exposed to
phosphoramide mustard, and these disparities suggested an uncoupling of the two
phenomena. Although sister chromatid exchange induction was not consistently
associated with cytotoxicity with the four agents, chromosome aberration
induction coincided with an inhibition of cell cycle kinetics in phosphoramide
mustard treated cells. The exceptionally high sister chromatid exchange
frequency of up to 21 times baseline in cells exposed to phosphoramide mustard
indicates that T-supressor lymphocytes stimulated with concanavalin A may be
particularly sensitive to the DNA-damaging effects of phosphoramide mustard.
Finally, these data suggest that the anticarcinogenicity of
2-mercaptoethanesulfonic acid correlates with its ability to attenuate
cytogenetic damage and cytotoxicity induced by reactive cyclophosphamide
metabolites.
The possible use of the degree of inhibition
of glutathione-S-transferase activity as a biological marker for determining
exposure to chemicals such as acrolein, styrene oxide, propylene oxide, ethylene
dibromide, and ethylene dichloride was explored. Glutathione-S-transferase
activity was studied in vitro in human erythrocytes or as the purified enzyme.
While glutathione-S-transferase activity was inhibited by all these compounds,
acrolein was the most inhibitory. A dose dependent inhibition was evident in
each case not only for inactivation of erythrocyte glutathione-S-transferase in
situ but for inhibition of purified erythrocyte glutathione-S-transferase as
well. Concentrations inhibiting 50% of the activity (I50) ranged from around
10(-3) to 10(-4) M. Some of the I50 values for the compounds used in this study
were relatively high. It was stated that the concentrations of these chemicals
in the blood of chronically exposed industrial workers may not reach these
levels. It is suggested that further studies be made to evaluate the usefulness
of inhibition of erythrocyte glutathione-S-transferase by these agents.
... Is a severe pulmonary irritant and
lacrimating agent with a piercing, disagreeable, acrid odor. It is ciliastatic
and capable of causing direct tissue damage ...
... Toxic effects of acrolein exposure include
sensory irritation, enzymatic inhibition, elevated liver alkaline phosphatase,
protein synthesis inhibition, weight loss, and death. Acrolein is a suspected
carcinogen ... May possess immunotoxic potential... Can induce pulmonary edema.
Severe irritation of the eyes, skin, mucous
membranes; abnormal pulmonary function; delayed pulmonary edema, chronic
respiratory disease.
Acrolein is a major contributor to the
irritative quality of cigarette smoke ...
Human Toxicity Values:
TCLo Man inhalation 1 ppm
Skin, Eye and Respiratory Irritations:
Acrolein produces intense irritation to the
eye and mucous membranes of the respiratory tract.
Intense lacrimation & nasal irritation ...
The general sequence of acrolein irritation is
concentration-time dependent eg, 1 ppm for 1 min gives slight nasal irritation;
1 ppm for 5 min gives intolerable eye irritation; 5.5 ppm for 5 seconds gives
moderate eye irritation; & 5.5 ppm for 1 min produces marked lacrimation.
...
Severe irritation of the eyes, skin, mucous
membranes; ... .
Acrolein is intensely irritating to the eyes
... . ... Skin irritation ... can be produced from prolonged or repeated
contact.
Medical Surveillance:
The monitoring of acrolein in the urine can be
accomplished through measurement of acrolein. This test may be useful for
identification of exposure. However, no information was located which showed a
correlation between urine levels and environmental exposure levels or the onset
of adverse health effects.
Respiratory Symptom Questionnaires:
Questionnaires have been published by the American Thoracic Society and the
British Medical Research Council. These questionnaires have been found to be
useful in identification of people with chronic bronchitis, however certain
pulmonary function tests such as FEV1 have been found to be better predictors of
chronic airflow obstruction.
Pulmonary Function Tests: The tests that have
been found to be practical for population monitoring include: Spirometry and
expiratory flow-volume curves; Determination of lung volumes; Diffusing capacity
for carbon monoxide; Single-breath nitrogen washout; Inhalation challenge tests;
Serial measurements of peak expiratory flow; Exercise testing.
Sputum Cytology: Sputum cytology along with
chest radiographs have been the standard procedures for detecting early lung
cancer in asymptomatic patients. Sputum cytology has been found to be useful for
detection of central tumors, especially squamous carcinomas.
Initial Medical Examination: A complete
medical history and physical examination with emphasis on the heart and lungs:
The purpose is to detect existing medical conditions which might place the
exposed employee at increased risk from reported effects of acrolein, and to
establish a baseline for future health monitoring. Examination of the heart and
lungs should be stressed. 14"x17" Chest roentgenogram: Acrolein may
cause lung damage. Surveillance of the lungs is indicated. Forced Vital Capacity
and Forced Expiratory Volume (1 sec): Acrolein is reported to cause decreased
pulmonary function. Periodic surveillance is indicated. Periodic Medical
Examination: The aforementioned medical examination should be repeated on an
annual basis, except that an x-ray is considered necessary only when indicated
by the results of the pulmonary function tests.
Populations at Special Risk:
Since acrolein has been shown to suppress
pulmonary antibacterial defenses, individuals with or prone to pulmonary
infections may also be at a greater risk /from exposure to this cmpd/.
Probable Routes of Human Exposure:
/In a 1974 report/, acrolein was detected in a
truck-maintenance shop in USA at a mean concn of 4.6 ug/cu m. The following
exposures to acrolein in workplace air have been reported: (1) levels of
0.44-1.5 mg/cu m ... in a Russian rubber vulcanization plant producing
styrene-butadiene rubber footwear components /from a 1969 report/; (2) 0.11-1.04
mg/cu (0.04-0.4 ppm) during the welding of metals coated with anti-corrosion
primers /from a 1973 report/; (3) 0.22-0.32 mg/cu m in pitch-coking plants,
0.004-0.014 in coal-coking plants /from a 1972 report/; and (4) less than 0.1
mg/cu m (0.04 ppm) from diesel train engine exhaust during repair and servicing
/from a 1973 report/. Acrolein was found at quarries in exhaust gases from
diesel engines and in workplace air at levels of 2.1-7.2 mg/cu m /from a 1981
report/.
NIOSH (NOES Survey 1981-1983) has
statistically estimated that 65 workers are exposed to acrolein in the USA(1).
However, this estimate does not include exposure to tradename compounds which
contain acrolein. Occupational exposure to acrolein may occur through inhalation
and dermal contact with this compound at workplaces where acrolein is produced
or used(SRC). Exposure of the general population occurs primarily through
atmospheric contact(1). The variety of outdoor and indoor sources includes
incomplete combustion of fuels and other organic compounds, production and
manufacturing processes, photochemical oxidation of airborne hydrocarbons, and
cigarette smoke (both first- and secondhand)(2). Despite different sources,
typical atmospheric concentrations (1- 20 ppb) usually differ little between
indoor and outdoor air(2).
Minimum Fatal Dose Level:
INHALATION OF AIR CONTAINING 10 PPM ACROLEIN
MAY BE FATAL IN A FEW MIN.
Antidote and Emergency Treatment:
Flush eyes with abundant water, also wash
thoroughly contaminated skin using soap. Treat skin burns as usual. Supply
oxygen with use of intermittent positive-pressure breathing apparatus. ...
Contaminated clothing should be promptly removed ... .
Exposure should be treated with copious
irrigation; ...
Basic treatment: Establish a patent airway.
Suction if necessary. Watch for signs of respiratory insufficiency and assist
ventilations if necessary. Administer oxygen by nonrebreather mask at 10 to 15
L/min. Monitor for pulmonary edema and treat if necessary ... . For eye
contamination, flush eyes immediately with water. Irrigate each eye continuously
with normal saline during transport ... . Do not use emetics. For ingestion,
rinse mouth and administer 5 ml/kg up to 200 ml of water for dilution if the
patient can swallow, has a strong gag reflex, and does not drool. Administer
activated charcoal ... . Cover skin bums with dry sterile dressings after
decontamination ... . /Acrolein and related compounds/
Advanced treatment: Consider orotracheal or
nasotracheal intubation for airway control in the patient who is unconscious or
in severe respiratory distress. Positive pressure ventilation techniques with a
bag valve mask device may be beneficial. Consider drug therapy for pulmonary
edema .... Monitor cardiac rhythm and treat arrhythmias if necessary ... . Start
an IV D5W /SRP: "To keep open", minimal flow rate/. Use lactated
Ringer's if signs of hypovolemia are present. Watch for signs of fluid overload.
Use proparacaine hydrochloride to assist eye irrigation ... . /Acrolein and
related compounds/
Animal Toxicity Studies:
Toxicity Summary:
Acrolein is very toxic to aquatic organisms.
Acute EC50 and LC50 values for bacteria, algae, crustacea, and fish are between
0.02 and 2.5 mg/liter, bacteria being the most sensitive species. ... In animals
and humans the reactivity of acrolein effectively confines the substance to the
site of exposure, and pathological findings are also limited to these sites. ...
Acrolein reacts directly with protein and non-protein sulfhydryl groups and with
primary and secondary amines. It may also be metabolized to mercapturic acids,
acrylic acide, glycidaldehyde or glyceraldehyde. Evidence for the last three
metabolites has only been obtained in vitro. Acrolein is a cytotoxic agent. In
vitro cytotoxicity has been observed as low as 0.1 mg/liter. The substance is
highly toxic to experimental animals and humans following a single exposure via
different routes. The vapor is irritating to the eyes and respiratory tract.
Liquid acrolein is a corrosive substance. ... At higher single exposure levels,
degeneration of the respiratory epithelium, inflammatory sequelae, and
perturbation of respiratory function develop. ... In general, body weight gain
reduction, decrement of pulmonary function, and pathological changes in nose,
upper airways, and lungs have been documented in most species exposed to
concentrations of 1.6 mg/cu m or more for 8 hr/day. Pathological changes include
inflammation, metaplasia, and hyperplasia of the respiratory tract. Significant
mortality has been observed following repeated exposures to acrolein vapor at
concentrations above 9.7 mg/ cu m. In experimental animals acrolein has been
shown to deplete tissue glutathione and in in vitro studies, to inhibit enzymes
by reacting with sulfhydryl groups at active sites. There is limited evidence
that acrolein can depress pulmonary host defenses in mice and rats. Acrolein can
induce teratogenic and embryotoxic effects if administered directly into the
amnion. ... Acrolein has been shown to interact with nucleic acids in vitro and
to inhibit their synthesis both in vitro and in vivo. Without activation it
induced gene mutations in bacteria and fungi and caused sister chromatid
exchanges in mammalian cells. ... The threshold levels of acrolein causing
irritation and health effects are 0.7 mg/ cu m for odor perception, 0.13 mg/cu m
for eye irritation, 0.3 mg/ cu m for nasal irritation and eye blinking, and 0.7
mg/ cu m for decreased respiratory rate. ... In view of the high toxicity of
acrolein to aquatic organisms, the substance presents a risk to aquatic life at
or near sites of industrial discharges, spills and biocidal use.
Evidence for Carcinogenicity:
CLASSIFICATION: C; possible human carcinogen.
BASIS FOR CLASSIFICATION: Classification is based on increased incidence of
adrenal cortical adenomas to female rats and carcinogenic potential of an
acrolein metabolite. Acrolein is mutagenic in bacteria and is structurally
related to probable or known human carcinogens. HUMAN CARCINOGENICITY DATA:
None. ANIMAL CARCINOGENICITY DATA: Limited.
Evaluation: There is inadequate evidence in
humans for the carcinogenicity of acrolein. There is inadequate evidence in
experimental animals for the carcinogenicity of acrolein. Overall evaluation:
Acrolein is not classifiable as to its carcinogenicity to humans (Group 3).
Non-Human Toxicity Excerpts:
When swallowed, /acrolein/ produces severe
gastrointestinal distress with pulmonary congestion & edema.
SUBACUTE INHALATION TOXICITY OF ACROLEIN WAS
EXAM IN 4 GROUPS OF 20 HAMSTERS, 12 RATS, & 4 RABBITS EACH EXPOSED 6 HR/DAY,
5 DAYS/WK FOR 13 WK AT CONCENTRATIONS OF 0, 0.4, 1.4, & 4.9 PPM. THE HIGHEST
CONCENTRATION CAUSED DEATH IN RATS, OCULAR & NASAL IRRITATION, GROWTH
DEPRESSION & METAPLASIA & HYPERPLASIA OF THE LINING OF THE RESP TRACT IN
ALL SPECIES. THE LOWEST EXPOSURE LEVEL (0.4 PPM) PRODUCED NO TOXIC EFFECTS IN
RABBITS OR HAMSTERS.
Groups of pure bred beagle dogs, squirrel
monkeys (Saimiri sciurea), guinea pigs, & Sprague-Dawley derived rats were
exposed to 0.7 & 3.7 ppm (1.6 & 8.5 mg/cu m) acrolein vapor for 8 hr/day
on 5 days/wk for 6 consecutive weeks; squamous metaplasia & basal cell
hyperplasia in the trachea were observed in dogs & monkeys, & squamous
metaplasia of the lung in 7/9 monkeys.
ANIMAL EXPT INDICATE THAT ACROLEIN ...
/DESTROYS/ RESPIRATORY TRACT MUCOUS MEMBRANES TO SUCH AN EXTENT THAT RESPIRATORY
FUNCTION IS FULLY INHIBITED WITHIN 2-8 DAYS.
/ACROLEIN/ ... AFFECTS ALKALINE PHOSPHATASE
& TYROSINE-ALPHA-KETOGLUTARATE TRANSAMINASE ACTIVITIES IN RATS 5-12 HR AFTER
INJECTION (3 MG/KG 20 HR BEFORE SACRIFICE) OR INHALATION. ... DATA SUGGESTED ...
ACROLEIN STIMULATES PITUITARY-ADRENAL SYSTEM, LEADING TO HYPERSECRETION OF
GLUCOCORTICOIDS ... /WHICH STIMULATE SYNTH OF ENZYME PROTEINS/.
Acrolein has ... been reported to cause
alterations in lung & liver biochemistry, incl significant reduction in
microsomal mixed-function oxidase activity, in rats given 2 ip injections of 5
mg/kg body wt acrolein. A single ip injection of 3 mg/kg body wt acrolein to
male Holtzman rats ... caused a prolongation of ... pentobarbital &
hexobarbital sleeping time. In vitro studies ... total destruction of liver
& lung microsomal the reduced form of nicotinamide-adenine dinucleotide
phosphate cytochrome c reductase by 1.5 to 6 mM (0.084 to 3.3 mg/ml) acrolein,
total loss of nonprotein sulfhydryl content & partial loss of protein
sulfhydryl content in these organs /have been observed/. Depletion of sulfhydryl
(21-63%) in the resp mucosa of male Fisher 344 rats after inhalation of 0.1 to 5
ppm (0.23 to 11.5 mg/cu m) acrolein vapor has ... been reported.
Two groups of 18 male & female Syrian
golden hamsters, 6 wk old, were exposed to 0 or 4 ppm (0 or 9.2 mg/cu m)
acrolein vapor (purity unspecified) for 7 hr/day on 5 days/wk for 52 weeks. Six
animals per group were killed at 52 wk & the remainder at 81 wk. Survival
was similar in treated & control animals. No tumor of resp tract was found
in any group.
... ACROLEIN INDUCED MUTATIONS IN DROSOPHILA
MELANOGASTER (2.23% COMPARED TO 0.19% IN CONTROLS). ... RESULTS REPORTED ...
INDICATE THAT ACROLEIN IS MUTAGENIC IN AN ESCHERICHIA COLI STRAIN DEFICIENT IN
DNA POLYMERASE WITHOUT METABOLIC ACTIVATION.
IT WAS ... NEGATIVE IN BACK-MUTATION TEST
(SPOT TEST) WITH 2 YEAST STRAINS, 1 SENSITIVE TO BASE SUBSTITUTION (S211) &
1 TO FRAMESHIFT MUTATION (S128).
... /Acrolein/ added ... to an in vitro rat
embryo culture at 5 ug/ml (equimolar to a teratogenic dose of cyclophosphamide)
... /produced/ no growth retardation or increase in defects. At twice the dose
the cmpd was lethal. ... Growth retardation but no structural defects at 100
& 150 uM concentrations /were observed/ when rat embryos were exposed in
vitro. ...
Acrolein (practical grade), stabilized with
0.2% hydroquinone ... & dissolved in 25 ul of 0.9% sodium chloride, was
injected at doses of 0.001, 0.01, 0.1, 1.0 & 10 umol/egg (0.006 to 56 ug/egg)
into ... air space or the yolk sac of 3-day-old White Leghorn SK 12 strain chick
embryos. On day 14 of incubation, the embryos were examined for ... viability
& malformations. Dose-related lethality was observed ... . No clear evidence
of teratogenic potential was found.
Dose-related incr in embryolethality, but not
in malformations (4/69 fetuses at high dose, compared to 2/121 in control group
were malformed, but this difference was not significant), was found when groups
of New Zealand white rabbits were injected iv on day 9 of gestation with 3, 4.5
or 6 mg/kg body wt acrolein (stabilized with 0.2% hydroquinone). The high dose
killed 6/16 rabbits, compared to 0/13 controls. ... Direct injections into yolk
sac of 10, 20 or 40 ul of a 0.84% soln of acrolein in physiological saline into
day-9 embryos resulted in a dose-related incr in ... resorptions (63% in
high-dose group compared to 21.2% in controls) & malformations (23.3% in
high-dose group compared to 3% in controls). The defects in high-dose group incl
hypoplastic & asymmetrical cervical & thoracic vertebrae, shortened
extremities & a ventricular septal defect.
Signs of ... /toxicity in mallard ducks given
oral LD50 doses of acrolein/. Regurgitation, reluctance to leave the swimming
pond, slow responses, ataxia, geotaxia, imbalance, phonation, wing tremors,
running & falling, asthenia, myasthenia, & withdrawal. Treatment levels
as low as 3.33 mg/kg /orally/ produced /these/ signs /in mallards/. Signs
appeared as soon as 10 min & persisted up to 36 days after treatment.
Mortalities occurred as soon as 32 min; However, several mortalities occurred
several days after treatment. /Sample purity: 92%/
Repeated inhalation by chickens of 50 &
200 ppm (115 & 450 mg/cu m) acrolein vapor for 5 min/day for 1 to 27 days
produced concentration-dependent decreases in the numbers of ciliated &
goblet cells & mucous glands in the trachea, & lymphocytic inflammatory
lesions in the tracheal mucosa.
Lesions occurring in the respiratory tract of
mice after exposure to 10 sensory irritants, incl acrolein, at a concn which
elicited a respiratory rate decr of 50% (RD50 of acrolein= 1.7 ppm), were
compared with respect to type and severity. After exposure of mice for 6 hr/day
for 5 days, the respiratory tract was examined for histopathological changes.
All irritants produced lesions in the nasal cavity with a distinct
anterior-posterior severity gradient. The lesions ranged from slight epithelial
hypertrophy or hyperplasia to epithelial erosion, ulceration, and necrosis with
variable inflammation of the subepithelial tissues.
Groups of Fischer 344 rats were exposed to
either filtered air, 0.4, 1.4, or 4.0 ppm acrolein for 62 days (6 hr/day, 5
days/wk). Mortality was observed only in the 4.0 ppm chamber, where 32 of 57
male rats died, but none of the 8 exposed females died. The lungs of the 4.0 ppm
group were heavier than those of the larger control animals. Relative to
controls, there was a 20% incr in total dry lung wt while the percent dry wt
decr 1.5% in the high dose group. Lung connective tissue content was incr as a
result of subchronic acrolein exposure. The amount of elastin per unit dry wt
was 173% of control values in the animals exposed to 4.0 ppm acrolein. Collagen
levels were elevated in both the 1.4 and 4.0 ppm groups, 113 and 137%,
respectively, of control values. Histologically, the 4.0 ppm animals
demonstrated bronchiolar epithelial necrosis and sloughing, bronchiolar edema
with macrophages, and focal pulmonary edema. Exposure related lesions were
observed in only 3 of the 31 rats examined from the 1.4 ppm chamber and in none
of the animals exposed to 0.4 ppm acrolein.
Continuous 90 day exposure at 0.22 ppm caused
inflammation in liver, lung, kidneys, and heart of monkeys, guinea pigs, and
dogs. Exposure to 1.8 ppm caused squamous cell metaplasia and basal cell
hyperplasia of the trachea in monkeys.
Inhibition of cell multiplication starts at
0.44 mg/l in protozoa (Uronema parduczi Chatton-Lwoff); At 0.21 mg/l in bacteria
(Pseudomonas putida); And at 0.04 mg/l in algae (Microcystis aeruginosa). The
lowest observed avoidance concn in insects was above 0.1 mg/l for mayfly nymphs
(Ephemerella walkeri); 0.1 mg/l for rainbow trout (Salmo gairdneri). The
incipient Median Threshold Limit (TLm) for fathead minnow was 84 ug/l in a flow
through bioassay; The maximum acceptable toxicant concentration was 11.4 ug/l.
The pathologic and immunotoxic effects of
acrolein were studied using 4 groups of male Sprague-Dawley rats. Rats were
exposed to 0, 0.17, 1.07, or 2.98 ppm of acrolein for 6 hr/day, 5 days/wk for 3
wk. From each treatment group (N= 40), 12 rats were used for spleen and lung
associated lymph node blastogenesis using the T-cell mitogen, phytohemaglutinin
P, and the B-cell mitogen, Salmonella typhimurium. Ten additional rats received
an intratracheal challenge of sheep erythrocytes after which lung associated
lymph node cells were assayed for plaque formation. The remaining 18 rats were
evaluated for host resistance to Listeria monocytogenes. Histological
examination of nasal turbinates of the rats exposed to 2.98 ppm revealed
exfoliation, erosion and necrosis of respiratory epithelium, and squamous
metaplasia. The lung did not demonstrate significant histopathology. A decrease
in body weight gain was observed only for rats exposed to 2.98 ppm. In vitro
pulmonary immune response as determined by the hemolytic plaque assay, and
lymphocyte response to phytohemaglutinin P and Salmonella typhimurium were not
affected by any of the acrolein exposures. Acrolein exposure did not affect
resistance to Listeria.
Acrolein is formed when fat is overheated and
has the typical smell of "burning fat". ... A poodle, shut up for half
an hour in a small unventilated kitchen with a chip pan of boiling fat, was seen
next day to have swollen tonsils, blood from the nostrils and a temperature of
39.4 deg C. 24 hr later there was slight dyspnea, the pulse was faint, the
tongue cyanosed and the eyes congested and discharging pus. It collapsed and
died soon afterwards.
Embryologic and teratogenic effects of
acrolein over a narrow concentration range in cultured rat embryos were
assessed. On the tenth day of gestation, pregnant Sprague-Dawley rats were
etherized and the uterus was removed. Embryos were dissected free of maternal
tissue and cultured in either a serum or serum free medium; dissolved acrolein
was added. After 42 hours of culture time, embryos were examined for viability
and morphology. For embryos cultured in serum, 100% mortality was observed at
140 uM acrolein. Significance in number of embryo deaths was reached at 120 uM;
median effective concentration (EC50) for embryo deaths was 115 uM. Significant
increases in embryo malformations were detected with doses as low as 80 uM; the
EC50 for malformations was 137 uM. Malformations of the brain, heart, somites,
facial area, and forelimb buds occurred most frequently. Doses of 80 uM acrolein
and greater produced significant decreases in embryo growth and development.
Yolk sac diameter, crown rump length, head length, number of somites, protein
content, and total morphological score decreased significantly at 120 uM
compared to controls. In embryos cultured in a serum free medium, acrolein was
totally embryolethal at 20 uM; EC50 for acrolein induced mortality was 8.3 uM.
Malformations occurred in 67, 80, and 100% of the embryos in the 5, 10, and 15
uM dose groups, respectively. The EC50 for acrolein induced malformations was
2.8 uM. Malformations included reduced left forelimb bud, blebs of the
maxillary, nasal or optic region, protrusions of the body, hindlimbs or head
area, cardiac malformations, head abnormalities, incomplete turning, and
irregular somites. At 5 and 10 uM acrolein, there was a significant decrease in
yolk sac diameter, crown rump and head length, somite number, and morphological
score.
The mutagenic potential of acrolein has been
studied with a wide range of in vitro and in vivo genetic toxicity assays. The
data often have been conflicting, especially with the Ames assay. This study was
undertaken to assess the mutagenic potential of acrolein using the CHO/HGPRT
assay, both with and without metabolic activation. This assay system was chosen
because it provides eukaryotic DNA as the target and is capable of detecting a
range of mutational events. Because of its considerable toxicity, acrolein was
tested over a very narrow dose range of 0.2-2 nl/ml without exogenous activation
and 0.5-8 nl/ml with rat S-9 activation. Multiple assays were performed under
both conditions. The results indicated that while acrolein was clearly very
cytotoxic, it did not induce a significant mutagenic response in the presence or
absence of metabolic activation.
The effect of systemic administration of
acrolein, a constituent of cigarette smoke and a metabolite of cyclophosphamide,
on the urinary bladder epithelium of 8 week old male F344 rats was investigated.
The animals were injected with single dose of acrolein at 25 mg/kg by
intragastric intubation or ip injection. The 25 mg/kg dose level proved
extremely toxic. The mortality rate was 42% for both groups. Rats administered
acrolein intragastrically had severe erosive hemorrhagic gastritis. Rats treated
ip had severe localized peritonitis. Surviving animals were sacrificed at 24 or
48 hours after administration and shown to have focal simple hyperplasia of the
urinary bladder after 2 days. In a second set of studies groups of 10 week old
male F344 rats were given acrolein via intraperitoneal injection at doses of
0.5, 1, 2, 4, or 6 mg/kg divided into up to three doses. Rats were injected with
tritiated thymidine 7 days after the first treatment, and bladders were
processed for autoradiographic evaluation. Sufficient acrolein reached the
urinary bladder to induce a proliferative response following ip administration
as determined by autoradiography.
The carcinogenic effects of chronic exposure
to acrolein, acrolein diethylacetal, acrolein oxime, and allyl alcohol were
tested in rats and hamsters. Each compound was administered at various doses up
to near the maximum tolerated dose in drinking water to groups of 20 male or
female F344 rats for up to 2 years. Acrolein was not given to hamsters because
it proved to be too toxic for administration in an adequate dose. The other
compounds were given at doses of 2 mg/wk by gavage to male Syrian golden
hamsters. One group of each species was maintained as untreated controls, and a
group of rats was given acetaldoxine as a control for possible carcinogenicity
of oximes. Animals that survived the treatments were allowed to die naturally or
were killed when moribund, and they were necropsied and lesions examined
histologically. There was little or no effect of any of the treatments on
mortality of the rats compared with the controls. The only suggestion of a
possible carcinogenic effect was an unusually high incidence of five adenomas
and two hyperplastic nodules of the adrenal cortex in the group of 20 rats
treated with the highest concentration (625 ppm) of acrolein. The incidence of
common neoplasms was very similar to the incidence in the controls. Three
hamsters had adenomas of the pancreatic ducts, which were not seen in untreated
hamsters. Approximately half of the hamsters treated with acrolein diethylacetal
or acrolein oxime that survived early toxicity died with neoplasms. It was
concluded that, considering the relatively small size of the test groups, it is
not certain that acrolein and its derivatives are not carcinogenic, although it
appears that any carcinogenic effect of these compounds will be weak.
Acrolein has been shown to form cyclic
deoxyguanosine adducts when it reacts with DNA in vitro. In this study, a
recently developed immunoassay for these adducts to study their formation in DNA
from Salmonella typhimurium exposed to acrolein /was utilized/. Acrolein
deoxyguanosine adducts were formed in a dose dependent fashion in Salmonella
tester strains TA100 and TA104, reaching levels as high as 5 umol adduct/mol
deoxyguanosine. Using the liquid preincubation assay, acrolein induced mutations
were also found in strains TA100 and TA104. The correlation between acrolein
deoxyguanosine adduct concentration and acrolein induced mutations in TA100,
which contains GC base pairs at the site of reversion, suggests that the
acrolein deoxyguanosine adduct is a promutagenic lesion. That mutations are also
seen in TA104 which contains AT base pairs at the site of reversion suggest that
adducts of bases other than deoxyguanosine may also be important in the
mutagenic activity of acrolein.
The effects of acrolein were studied on the
chick embryos of 48 and 72 hr of incubation. Acrolein was dissolved in
physiological saline and injected into the air sacs of the eggs at doses ranging
from 0.001 to 0.1 mg per egg. The controls received an equal amount of saline
only (0.1 ml per egg). All the embryos including controls were examined at day
13. In all, 600 eggs were utilized for this investigation. At 48 hr incubation,
the percentage survival ranged from 80 to 0 as the dosage of acrolein was
increased. Embryonic mortality following 72 hr incubation did not increase
significantly at any dose level. Gross malformations such as short and twisted
limbs, everted viscera, microphthalmia, short and twisted neck, and hemorrhage
over the body were observed. The frequency and the type of gross abnormalities
did not vary much in the 48 or 72 hr treated groups. The incidence of
malformation in the controls was low. The results of this study indicate that
acrolein is embryotoxic at higher doses and moderately teratogenic to chick
embryogenesis.
An animal model was used to study the effects
of early administration of intramuscular corticosteroids on mortality and lung
histopathology induced by a component of smoke. Thirty-six rabbits (mean weight,
2.7 kg) were exposed to acrolein vapor for 15 min; 30 min later the animals were
divided into 3 treatment groups. One group received saline placebo
intramuscularly at 12 hr intervals, a second group was treated intramuscularly
with 100 mg methylprednisolone at 12 hr intervals, and a third group was treated
with a single 100 mg dose of methylprednisolone followed by doses of saline at
12 hr intervals. The animals were studied for a 72 hr period. There was a
significantly lower mortality in the 2 steroid-treated groups than in the
nontreated group. A scoring system was developed for evaluating observed
histologic changes in the lung. No correlation was seen between survival and
histologic score or between score and treatment. High scores for particular
histologic features did not explain mortality nor did they predominate in
untreated animals; vascular congestion was found to be greater in the
steroid-treated group. The beneficial effects of steroids in reducing mortality
after inhalation of a common smoke constituent was not associated with any
evidence of attenuation of lung damage.
... Acrolein at concn of 1x10-4 to 1x10-10 M
was phytotoxic to tobacco tissue cultures.
Acrolein is a direct-acting mutagen in
prokaryotic and eukaryotic systems...
Non-Human Toxicity Values:
LD50 Rat oral 46 mg/kg
LD50 Rat sc 50 mg/kg
LD50 Mouse sc 30 mg/kg
LD50 Rabbit oral 7 mg/kg
LD50 Rabbit skin 562 mg/kg
LC50 Sprague-Dawley rat (combined sexes) 26
ppm/1 hr
LC50 Sprague-Dawley rat (combined sexes) 8.3
ppm/4 hr
LD50 Cat inhalation 11 ppm/3-10 hr
LD50 Cat inhalation 18-92 ppm/3-4 hr
LD50 Cat inhalation 690-1150 ppm/2 hr
LD50 Rat inhalation 130 ppm/30 min
Ecotoxicity Values:
LD50 Mallard Duck (male, 3-5 mo old) oral 9.11
mg/kg (95% confidence limit 6.32 mg/kg) /Sample purity 92%/
LD50 Carassius auratus (goldfish) <0.08
mg/l/24 hr (modified ASTM D 1345) /Conditions of bioassay not specified/
LC50 Lepomis macrochirus (bluegill sunfish) 79
ug/l/24 hr /Conditions of bioassay not specified/
LC50 Salmo trutta (brown trout) 46 ug/l/24 hr
/Conditions of bioassay not specified/
LC50 Lepomis macrochirus 0.10 mg/l/24 hr ;
0.09 mg/l/96 hr /Conditions of bioassay not specified/
LC50 Daphnia magna 0.23 mg/l/24 hr; 0.083
mg/l/48 hr; No discernible effect conc= 0.034 mg/l. /Conditions of bioassay not
specified/
CARP & THREAD-FIN SHAD ARE PARTICULARLY
SENSITIVE, BEING KILLED @ 1 TO 2 PPM. BLACK BASS, BLUE GILL, & LAMPREY EEL
LARVAE APPEAR TO TOLERATE UP TO 5 PPM. /CONDITIONS OF BIOASSAY NOT SPECIFIED/
Inhibition of cell multiplication starts at
0.44 mg/l in Uronema parduczi (protozoa). ...
The lowest observed avoidance concn in insects
was above 0.1 mg/l for Ephemerella walkeri (mayfly nymphs) ... .
... The incipient Median Threshold Limit (TLm)
for Pimephales promelas (fathead minnow) was 84 ug/l in a flow through bioassay;
The maximum acceptable toxicant concentration was 11.4 ug/l.
LC50 Pimephales promelas (fathead minnow) 14.0
ug/1/96 hr (confidence limit not reliable), flow-through bioassay with measured
concentrations, 17.4 deg C, dissolved oxygen 9.3 mg/l, hardness 45.2 mg/l
calcium carbonate, alkalinity 42.9 mg/l calcium carbonate, and pH 7.4.
LC50 Pimephales promelas (fathead minnow) 19.5
ug/1/96 hr (confidence limit 17.3-22.0 ug/l), flow-through bioassay with
measured concentrations, 24.9 deg C, dissolved oxygen 7.3 mg/l, hardness 45.0
mg/l calcium carbonate, alkalinity 44.1 mg/l calcium carbonate, and pH 7.9.
EC50 Pimephales promelas (fathead minnow) 19.5
ug/l/96 hr (confidence limit 17.3-22.0 ug/l), flow-through bioassay with
measured concentrations, 24.9 deg C, dissolved oxygen 7.3 mg/l, hardness 45.0
mg/l calcium carbonate, alkalinity 44.1 mg/l calcium carbonate, and pH 7.9.
Effect: Affected fish lost schooling behavior, were hyperactive and overreactive
to external stimuli, and had increased respiration. Equilibrium loss was not
observed prior to death.
Inhibition of cell multiplication starts at
... 0.21 mg/l in bacteria (Pseudomonas putida) ...
Inhibition of cell multiplication starts at
... 0.04 mg/l in algae (Microcystis aeruginosa). ...
Ongoing Test Status:
The NTP Toxicology Research and Testing
Program releases a Management Status Report on a quarterly basis. This report
gives the status of chemicals studied, under study, or proposed for study by NTP.
The 07/11/2001 issue indicates that short term toxicity study on acrolein is
scheduled for peer review. Route: gavage; Species: rats and mice. NTP TR No 48.
TSCA Test Submissions:
Acrolein (CAS # 107-02-8) was evaluated for
acute oral toxicity in groups of 10 male CD-1 mice administered single doses of
0.0, 11.0, 13.2, 15.84, and 19.0 mg/kg by oral gavage (10 ml/kg in deionized
water). Treatment was associated with lethargy, squinting of eyes, rough coats,
hunching, and piloerection. Several survivors of 14-day post-gavage observation
also had blackening, necrosis, and breakage of nails. Reduced weight gains
(-11.6% - 28.6%) persisted at all dose levels to 14th-day end of study. All
treatment-related mortality (22/50) occurred within 2 days of dosing and was
consistent with an oral LD50 (by Karber probit analysis) in male mice of 13.9
(95% confidence limit, 12.8 - 15.1) mg/kg. Upon necropsy, the study lethalities
exhibited reddened lungs and hemorrhagic stomachs and intestines. Other than 1
male of a 13.2 mg/kg dose with reddened lungs, the study survivors showed
minimal pathological changes on terminal sacrifice.
Acrolein (CAS # 107-02-8) was evaluated for
mutagenicity in the Salmonella Liquid Suspension Mutant Fraction Assay. Relative
to negative control, concentrations of 1, 3, 10, 20, and 40 ug/ml induced no
concentration-related mutagenicity (increased mutant fraction, or number of
mutants/viable cell) in duplicate assays with 5 Salmonella strains, either with
or without rat liver metabolic activation.
Acrolein (CAS # 107-02-8) was evaluated for
acute oral toxicity in groups of 10 nonfasted male rats albino administered
doses of 0, 31.6, 39.8, 50, and 63 mg/kg by oral gavage. Based on a method of
Thompson, treatment was associated with an oral LD50 for male rats of 46 (39 -
56) mg/kg. Doses of 46 mg/kg administered to rats in a 0.05% aqueous dilution
(instead of 0.5%) killed only 1/10 rats in a subsequent trial. Study lethalities
had congested and mottled livers, hemorrhagic peritoneums, and hemorrhagic and
injected stomachs.
Acrolein (CAS # 107/02-8) was evaluated for
acute oral toxicity in groups of 5 male New Zealand albino rabbits fed single
doses of 3.16, 6.3, 12.6, and 25.2 mg/kg (1% in water). Treatment was associated
with mortality consistent with an oral LD50 in rabbits of 7.1 (3.1 to 16.7)
mg/kg. No further information was provided. Study lethalities had pale and
mottled livers, injected, congested and hemorrhagic stomachs, and pale and
friable kidneys.
Acrolein (CAS # 107-02-8) was evaluated for
repeated dose oral toxicity in groups of 10 Sherman strain rats exposed to
concentrations of 0, 1, and 10 ppm in the drinking water (approximate doses of
0, 0.17, and 1.5 mg/kg/day) for 30 days. Treatment was associated with decreased
fluid ingestion, reduced mean weight gain in surviving rats, and increased
relative kidney weights (10 ppm), with no increased toxic mortality or
pathology. Histopathological evaluation of small intestine, kidney, and liver
revealed no treatment-related changes. Two day trial with exposures to 0, 30,
100, 300, and 1000 ppm in the drinking water versus fluid imbibed in groups of
10 rats revealed that reduced fluid intake is significantly related to acrolein
concentrations.
Acrolein (CAS # 107-02-8) was evaluated for
acute inhalation toxicity in Sprague-Dawley rats (5/sex/group) administered
single dynamically-generated exposures to mean vapor concentrations of 0, 14,
22, 24, 31, and 81 ppm for 1 hour or 0, 4.8, 7.0, 9.1, and 12.1 ppm for 4 hours.
Exposures were associated with clinical signs of toxicity at all exposure
levels, including lacrimation, periocular, perinasal, and perioral wetness and
encrustation, unkempt fur, labored breathing, lethargy, and stomach distention.
Body weights or bodyweight gains were universally depressed during post-exposure
Week 1 and, during Week 2, in 22 and 24 ppm groups of 1-hour exposures and 12.1,
9.1, and 7.0 ppm groups of 4-hour exposures. Treatment-related mortality
occurred primarily from Day 1 through Day 6 and, based on a Thompson moving
average method, was consistent with all-sex inhalation 1-hour and 4-hour LC50s
(with 95% confidence limits), respectively, of 26 (24-27) ppm and 8.3 (7.0-9.9)
ppm. Upon necropsy, gross lesions were identified only in study lethalities and
included perinasal and perioral encrustation, mottled discoloration of lungs and
liver, clear fluid-filled trachea and thoracic cavity, reddened submandibular
lymph nodes, gas-filled stomach and intestines, and opaque or cloudy eyes.
Acrolein (CAS # 107-02-8) was evaluated for
mutagenicity in the Chinese Hamster Ovary (CHO) Mutation test. Selected based on
preliminary cytotoxicity tests, concentrations of 0.0 (ethanol solvent control),
0.2, 0.5, 1.0, 2.0, and 4.0 x 10(-5)% (v/v), both in the presence and the
absence of S9 metabolic activation, produced statistically significant
(Student's t-test, p < 0.01) mutagenicity (mutants/10(6) cells/viable cells).
Significantly increased CHO mutagenicity, ranging from 56.2 (2.0 x 10(-5)%) to
200.00 (0.5 x 10(-5)%) mutants/10(6) viable cells without metabolic activation
and 18.6 (0.2 x 10(-5)%) to 190.9 (2.0 x 10(-5)% mutants/10(6) viable cells, did
not correlate to concentrations, however, and positive results were not obtained
in either Sister Chromatid Exchange or Unscheduled DNA Synthesis tests. While
acrolein mutagenicity was statistically indicated in the CHO Mutation test, a
dose-response relationship was not demonstrated.
Acrolein (CAS # 107-02-8) was evaluated for
clastogenicity in the Sister Chromatid Exchange (SCE) test. Selected based on
preliminary cytotoxicity tests, 6 staggered acrolein concentrations between 0.0%
(negative culture, ethanol solvent, and positive controls) and 3.0 x 10(-5)%
(v/v) without S9 metabolic activation and between 0.0% and 10.0 x 10(-5)% with
metabolic activation, respectively, induced no statistically significant
(Student's t-test) dose-related increments in Chinese Hamster ovary (CHO) cell
SCE frequency (SCE/cell, mean SCE/chromosome of 20 cells/culture) after 5-hour
and 2-hour incubations. Statistically significant increases in SCE were observed
at doses of 0.8 x 10(- 5)% (p < 0.05) and 5.0 x 10(-5)% (p < 0.01),
respectively, in cultures without and with S9 metabolic activation; however,
based on a lack of a dose-response relationship, study authors concluded that
acrolein does not induce SCE-derived mutagenicity in vitro.
Acrolein (CAS # 107-02-8) was evaluated for
mutagenicity in an Unscheduled DNA Synthesis (UDS) Assay with rat hepatocytes.
Selected based on preliminary cytotoxicity tests, 12 acrolein concentrations
from 0.00 (ethanol solvent control, 2 positive controls) to 30.0 x 10(-5)% added
to rat liver cells cultured in the presence of 3H-thymidine and hydroxyurea for
2 hours were associated a statistically significant (p < 0.05, Duncan's
Multiple Range Analysis) increase in nuclear-bound label per 10(6) viable
hepatocytes at a dose of 0.6 x 10(5)%. Further, both nuclear-bound label and
DNA-bound label from DNA precipitated per 10(6) viable hepatocytes/dose exposed
at toxicity levels allowing at least 50% survival were consistently numerically
greater than values obtained from historical and solvent controls. A lack of
dose-related statistically significant increases in either nuclear- and/or
DNA-bound label led authors to conclude this study was inconclusive regarding
acrolein-induced unscheduled DNA synthesis in rat hepatocytes in vitro.
Acrolein (CAS # 107-02-8) with several other
chemicals was evaluated for sensory (upper airway) irritation in a modified
Alarie Mouse Sensory Irritation Test. Four each male Swiss Albino CD-1 mice were
administered dynamic head only exposures to vapor concentrations of 0.0 to 8.7
ppm in air over 10 minutes to characterize type response as either immediate and
persisting, immediate with accommodation (ameliorated with time), or immediate
and progressive during exposures. Concentrations below 2 ppm produced a linear
response (breaths/minute/animal) curve, while maximal responses (decreased
respiration rate) occurred after 10 minutes' exposure, thus indicating a
progressive response to exposure without physiological accommodation or
compensation; an RD50 (linear regression determination of that concentration
causing 50% reduction of respiratory rate) was 1.27 ppm (R=0.89; 95% CL
1.07-1.52 ppm). Response data were not provided.
Acrolein (CAS # 107-02-8) was evaluated for
acute inhalation toxicity in groups of 5 each male and female Syrian golden
hamsters administered low dynamic whole-body exposures to vapor concentrations
of 11.2, 23.3, 30.0, and 30.4 ppm in air for 4 hours. During all exposures, the
animals kept their eyes shut and exhibited lachrymation, dyspnea, nasal
secretion, and, late in the exposure, inflating of cheek pouches. Treatment was
also associated with significantly dose-related mortality between 24 hours and
12 days post exposure, consistent with an LC50 (by a method of Litchfield and
Wilcoxon) of 25.4 ppm (58 mg/m3 air) with a calculated LCt50 of 101 ppm-hour.
Acrolein (CAS # 107-02-8) was evaluated for
acute inhalation toxicity in male Sprague-Dawley Spartan rats (7/exposure group)
administered single dynamically generated whole-body exposures to average
analytic vapor concentrations of 14.5, 41.5, 93.5, and 251 ppm for up to 30
minutes. During exposures and a 15-minute post-exposure venting period, the
animals were observed continuously for behavioral anomalies and sensory
irritation, including altered reflexes, eye and/or nasal irritation, and or
respiratory irregularities. Treatment was associated with clinical signs of
toxicity including teary and squinted eyes, nasal discharge, labored breathing,
gasping, and prostration at all levels of exposure; treatment also dampened
righting, blink, and pain reflexes at exposures of 41.5 ppm or greater.
Bodyweights were low normal based on comparison with historical controls, and
mortality was consistent with a 30-minute LC50 of 60 ppm. Additionally,
severity, time to onset, progression, and duration of the toxic response were
each correlated with dose. Immediate necropsy of study lethalities upon their
discovery revealed treatment-related gross pathology including congestion of
nasal turbinates (41.5 ppm), failure of lungs to collapse on incision with a
dark mottled and congested appearance of apical and cardiac regions of the lungs
(41.5 ppm, 1/7), accumulations of exudate around nose and mouth (93.5 ppm, 7/7;
251 ppm, 7/7), mucopurulent or mucohemorrhagic rhinitis (93.5 ppm, 7/7; 251 ppm,
7/7), pulmonary congestion and hemorrhage (93.5 ppm, 7/7; 251 ppm, 7/7), gaseous
distention of the stomach (93.5 ppm, 7/7; 251 ppm, 7/7), congestion of liver and
kidneys (93.5 ppm, 7/7; 251 ppm, 1/7), pulmonary edema (251 ppm), and
hydrothorax (251 ppm). None of 7/7 terminally sacrificed survivors of a 14.5 ppm
exposure exhibited any treatment-related gross pathology, while survivors of
41.5 ppm exposures had catarrhal rhinitis on Day 15 terminal necropsy.
Acrolein (CAS # 107-02-8) was evaluated for
subchronic inhalation toxicity in Syrian golden hamsters (10/sex/group)
administered dynamic whole-body exposures to vapor concentrations of 0, 0.4,
1.4, and 4.9 ppm in air for 6 hours/day, 5 days/week over 13 weeks. Treatment
with high and mid-level exposures was associated with clinical signs of
toxicity, including restlessness, insomnia, eye irritation, nasal discharge,
salivation, and statistically significant (p < 0.05, Student's t-test) and
persistent reductions in bodyweight (4.9 ppm). Treatment-related mortality
consisted of a solitary 4.9 ppm male killed in moribund condition in Week 12.
Elevations in hemoglobin and hematocrit values, as well as erythrocyte and
lymphocyte counts, were statistically significant (p < 0.05, Wilcoxon
analysis) in 4.9 ppm females, while the high-exposure female neutrophil count
was significantly depressed. Serum biochemistry values appeared unaffected in
both males and females, as urinalyses were unremarkable relative to controls.
Increased relative kidney, brain, gonad, and lung weights reached statistical
significance in high dose animals of both sexes, while relative heart weights
were significantly increased in 4.9 ppm females only. Examination of major
organs on terminal necropsy (on the day following a final exposure) revealed no
gross changes attributable to treatment, other than subcutaneous edema, ascites,
epididymal abscesses, gastric ulcer, and pale kidneys and liver of the
high-exposure male lethality. Histological evaluation of head, larynx, trachea,
and pulmonary lobes of each animal revealed cellular changes of the nasal
cavity, larynx, and trachea, including moderate rhinitis, necrosis, and hyper-
and metaplasia of respiratory and olfactory epithelium, primarily in the 4.9 ppm
group. Females of 4.9 ppm exposures also exhibited slight hyperplastic
appearance of the vocal cords and surrounding tissues and near universal focal
hyper- and metaplasia of the tracheal epithelium. A few males also showed
tracheal hyper- and metaplasia. No histopathological changes attributable to
acrolein exposure were identified in the bronchi or lungs, and, among the 4.9
ppm males and females examined, no other organ systems showed histological
manifestation of acrolein vapor toxicity. Only the premature high exposure study
lethality exhibited amyloidosis of the kidneys, liver, and adrenals, testicular
atrophy, as well as inflammatory changes in many organs.
Acrolein (CAS # 107-02-8) was evaluated for
mutagenicity in the Reverse Mutation Test using 5 strains of Salmonella
typhimurium cultured both in the presence and the absence of mammalian metabolic
activation with acrolein concentrations of 0 (negative and positive controls),
0.001, 0.01, 0.1, and 1.0 ug/plate (a dose of 10 ug was toxic in preliminary
screening tests) for 48 hours. None of the 5 Salmonella typhimurium strains
produced sufficiently increased revertants/plate over negative control to
indicate a acrolein mutagenicity and no dose-related response was demonstrated.
Acrolein (CAS # 107-02-8) was evaluated for
mutagenicity in a quantitative overlay assay using 5 strains of Salmonella
typhimurium cultured both in the presence and the absence of Aroclor-induced rat
liver microsomal enzyme with acrolein concentrations of 0 (solvent and positive
controls), 1, 3, 5, 10, 20, 30, and 50 ug/plate for 48 hours. None of the 5
Salmonella typhimurium strains produced sufficiently increased revertants/plate
over negative control, either with or without mammalian metabolic activation, to
indicate a acrolein mutagenicity. No toxicity was observed under these test
conditions, although preliminary screening had shown toxicity associated with
exposures to 25 to 39 ug/plate.
Metabolism/Pharmacokinetics:
Metabolism/Metabolites:
... The excretion of acrolein metabolites in
urine of adult female Wistar rats /was observed/ after a single oral admin of 10
mg/kg body wt acrolein in corn oil. S-carboxyethyl-N-acetylcysteine (S-carboxyethylmercapturic
acid) & S-(propionic acid methyl ester) mercapturic acid were reported to be
the major metabolites.
MALE CFE ALBINO RATS METABOLIZED 10.5% OF A SC
DOSE OF 1 ML OF A 1% SOLN OF ACROLEIN IN ARACHIS OIL TO
N-ACETYL-S-(3-HYDROXYPROPYL)-L-CYSTEINE, WHICH WAS ISOLATED FROM THE URINE.
Acrolein is metabolized in vitro by liver
& lung microsomes to glycidaldehyde.
Acrolein is a suspected carcinogen because of
its 2,3-epoxy metabolite ...
Absorption, Distribution & Excretion:
IT CAN ... BE ABSORBED PERCUTANEOUSLY ...
In goat and hen, no acrolein was detected in
tissues or excreta, or in goat milk or hen eggs following administration of high
doses.
Mechanism of Action:
ACROLEIN IS A GENERAL CELL TOXICANT, &
KILLS THROUGH ITS SULFHYDRYL REACTIVITY, WHICH DESTROYS VITAL ENZYME SYSTEMS IN
PLANT CELLS.
CARDIOVASCULAR ACTIONS OF ACROLEIN ADMIN IV
ARE SIMILAR TO ACETALDEHYDE & PROPIONALDEHYDE. PRESSOR RESPONSE APPEARS TO
RESULT FROM RELEASE OF CATECHOLAMINES FROM SYMPATHETIC NERVE ENDINGS & FROM
ADRENAL MEDULLA OF ANESTHETIZED RATS. THESE ALDEHYDES ALSO EXERT
CARDIOINHIBITORY EFFECT WHICH IS MEDIATED BY VAGUS NERVE. INHALATION STUDIES
WITH ACROLEIN REVEALED THAT THIS ALDEHYDE HAS SIGNIFICANT CARDIOVASCULAR
ACTIVITY AT CONCENTRATIONS BELOW THOSE WHICH MIGHT BE ENCOUNTERED IN CIGARETTE
SMOKE. PREDOMINANT EFFECT OF INHALED ACROLEIN AT THESE DOSES WAS AN INCREASE IN
BLOOD PRESSURE & HEART RATE.
Resting rat pulmonary alveolar macrophages
exposed to acrolein were stimulated to synthesize and release thromboxane B2 and
prostaglandin E2 in a dose-dependent manner. Although phagocytosis was also
inhibited in a dose-dependent manner, the reduction in prostaglandin E2 appeared
to be partially independent of particle ingestion since thromboxane B2 synthesis
was not affected by low doses of acrolein. In fact, high doses induced a slight
enhancement in thromboxane B2 synthesis. Therefore, acrolein selectively
inhibited the enzyme, prostaglandin endoperoxide E isomerase, necessary for the
conversion of the endoperoxide to prostaglandin E2. The possible involvement of
acrolein's sulfhydryl reactivity in the inhibition of the isomerase enzyme was
indicated. Pulmonary macrophages were unable to reverse the acrolein effects on
arachidonate metabolite synthesis after 6 hr in an acrolein-free environment.
EXPOSURE OF RABBIT LUNG ALVEOLAR MACROPHAGES
TO ACROLEIN INHIBITED PHAGOCYTOSIS, ADHESIVENESS, CALCIUM(2+)-DEPENDENT ATPASE,
BUT NOT MAGNESIUM(2+)-DEPENDENT ATPASE.
IN MICE EXPOSED TO ACROLEIN-FORMALDEHYDE
ATMOSPHERES, MEASUREMENT OF RESP RESPONSE SHOWED THAT ACROLEIN &
FORMALDEHYDE ACT AT SAME RECEPTOR SITE. COMPETITIVE ANTAGONISM OCCURS WHEN
PRESENT TOGETHER.
The inhibition of DNA-methylase activity by
acrolein was studied in vitro. DNA-methylase isolated from the urothelium or
liver of rats was incubated with acrolein and the extent of methylase inhibition
was determined. Acrolein at 10 umol/l inhibited liver DNA-methylase activity by
about 50% and urothelium activity by approximately 26%. A Line weaver-Burk plot
showed that acrolein inhibited liver DNA-methylase activity in a competitive
manner with an inhibition constant at 6.7 uM. Liver DNA-methylase was incubated
with 10 uM acrolein and 0 to 200 uM dithiothreitol or 0 to 50 uM glutathione and
the effects on DNA-methylase activity were determined. Glutathione and
dithiothreitol protected against acrolein induced inhibition of DNA-methylase
activity. Glutathione showed a much greater protective effect than
dithiothreitol. Hepatic DNA-methylase was incubated with acrolein in the
presence or absence of added DNA or methylase protein and the effects on DNA-methylase
activity were determined. Increasing the methylase protein concentration
protected against inhibition whereas increasing the concentration of DNA had no
effect. DNA/acrolein adducts from Micrococcus lysodeikticus were added to
hepatic DNA-methylase and the effect on DNA-methylase activity was investigated.
As the concentration of DNA adducts from Micrococcus lysodeikticus increased,
DNA-methylase activity decreased. The authors conclude that acrolein is similar
to N-methyl-N'-nitro-N-nitrosoguanidine in its ability to react with both DNA
and DNA-methylase protein.
Acrolein, a genotoxic aldehyde released in the
metabolic activation of the cytostatic drug cyclophosphamide, is inactivated by
glutathione transferases either by conjugation with reduced glutathione or by
covalent binding to the enzymes in the absence of glutathione or by covalent
binding to the enzymes in the absence of glutathione. The catalytic efficiency (kcat/Km)
with acrolein as a substrate was determined for representatives of the three
classes Alpha, Mu, and Pi of human glutathione transferases. Transferase pi
exhibited the highest and transferase epsilon the lowest catalytic efficiencies,
respectively. As measured by the kcat/Km value, acrolein ranks among the most
active substrates known for transferase Pi. The irreversible binding of acrolein
to the enzymes was monitored as the inactivation of the enzyme activity.
Transferase Pi reacted significantly more rapidly with acrolein than did
transferases Mu and epsilon.
An examination was conducted of the effects of
allylamine and acrolein on electron transport and oxidative phosphorylation in
mitochondria isolated from hearts of male Sprague-Dawley rats. Both acrolein and
allylamine inhibited State III, State IV, and uncoupler stimulated respiration
in a concentration dependent fashion when added to mitochondria respiring on
glutamate, malate, and malonate as substrate. While the concentration dependent
inhibitory effect was statistically greater for acrolein than allylamine for
State III and uncoupler stimulated oxygen uptake, the concentrations necessary
to produce these effects were in the millimolar range for both compounds.
Allylamine and acrolein also displayed concentration dependent effects on
respiratory enzyme activities in mitochondria actively respiring on succinate as
substrate. State III, State IV, and uncoupler stimulated oxygen uptake were
significantly inhibited by increasing concentration of all allylamine or
acrolein. In contrast to the results obtained with glutamate, malate, and
malonate, with succinate as substrate no significant differences between
allylamine and acrolein in concentration effect slopes were noted for State III,
State IV and uncoupler stimulated activities, indicating site selectivity
between the two compounds. Respiratory control ratios were significantly
decreased by allylamine and acrolein with glutamate, malate, and malonate
substrate. When succinate was used as substrate, the respiratory control ratio
was significantly reduced only by acrolein, again suggesting the site selective
nature of this compound.
Acrolein was evaluated in vitro as a potential
substrate or inhibitor of rat liver mitochondrial and cytosolic
aldehyde-dehydrogenases. Subcellular fractions, cytosolic and mitochondrial,
were prepared from male Sprague-Dawley rat livers without pretreatment and were
used on the same day they were prepared. Oxidation of acrolein by aldehyde
dehydrogenases in subcellular fractions and enzyme inhibition by acrolein were
assayed spectrophotometrically and chromatographically. It was found that
acrolein was not oxidized by either mitochondrial or cytosolic aldehyde
dehydrogenases, but rather was a potent inhibitor of these enzymes in a dose
dependent manner. In the presence of 2-mercaptoethanol, an adduct with acrolein
was formed and enzyme activity was detected. Particularly susceptible to the
inhibitory effects of acrolein was the mitochondrial high affinity aldehyde
dehydrogenase. Inhibition was rapid with an 88% reduction in control aldehyde
dehydrogenase activity within 5 seconds of addition of 10 uM acrolein. It was
suggested that at the aldehyde binding site an irreversible inhibition occurs
and at the cofactor binding site of the enzyme a reversible noncompetitive
inhibition occurs. Inhibition of cytosolic high affinity aldehyde dehydrogenase
was also rapid, with a 54% inhibition being reached in 5 seconds after addition
of 50 uM acrolein. It was concluded that acrolein may cause irreversible
inhibition of the isozymes by covalently binding to the sulfhydryl group through
a Michael addition to form a thioether at the active site of the enzyme. This
aldehyde dehydrogenase inhibitory effect of acrolein may be important in the
toxicity of aldehyde compounds liberated by lipid peroxidation. Acrolein
inhibition of aldehyde dehydrogenases may also be important in toxicities
associated with cyclophosphamide chemotherapy.
Acrolein is believed to cause tissue damage by
the mechanism of release of toxic /Oxygen/ radicals via activation of
arachidonic acid cascade, by binding to sulfhydryl groups, and by protein
damage.
Interactions:
The interaction of the antihypertensive agent
guanethidine and two aldehydes possessing sympathomimetic activity on the
pressure of spontaneously hypertensive rats was studied. Acrolein (0.05-0.5
mg/kg) produced a pressor response at low doses and a depressor response at high
doses in acutely and chronically guanethidine pretreated spontaneously
hypertensive rats. Depressor responses to high doses of aldehydes may have been
attributed to vagal stimulation or direct vasodilation. There was a significant
interaction between the aldehydes and guanethidine, which may have implication
for someone undergoing treatment with guanethidine for hypertension while being
exposed to acetaldehyde and related cmpd from ethanol and tobacco smoke.
Muramyl dipeptide protection from acrolein
toxicity was tested using isolated rat hepatocytes. Incubation of hepatocyte
suspensions with acrolein (143 umol/ml) for 15 min reduced viability to 62%.
Pretreatment of hepatocytes in incubation media with muramyl dipeptide (20.6
nmol/ml) incr viability significantly to 83% p<0.05). It is suggested that
muramyl dipeptide in certain dosages may produce nonspecific stabilization of
cytoplasmic membranes towards acrolein.
The protective effect of n-acetylcysteine
against the toxicity of ... acrolein ... was investigated using isolated rat
hepatocytes as the experimental system. ... n-Acetylcysteine protected against
acrolein toxicity by providing a source of SH groups, and was effective without
prior conversion.
Groups of 30 male & 30 female Syrian
golden hamsters were exposed to 0 or 4 ppm (0 or 9.2 mg/cu m) acrolein vapor
(purity unspecified) for 7 hr/day on 5 days/wk for 52 weeks, & were given,
at the same time & also for 52 wk, weekly intratracheal instillations of 2
dose levels of benzo(a)pyrene or sc injections of n-nitrosodiethylamine (once
every 3 wk). All surviving animals were killed at 81 wk. Addnl exposure to
acrolein did not significantly incr the tumor incidence produced by
benzo(a)pyrene or N-nitrosodiethylamine.
/Male Sprague-Dawley albino/ rats were exposed
to experimental atmospheres of carbon monoxide in air, acrolein in air, and to
mixtures of carbon monoxide and acrolein in air. The toxic potency of each ...
was evaluated ... by measurement of time to incapacitation as a function of
toxic gas concentrations. ... There was no evidence of synergistic action. ...
An inhibitory or antagonistic effect of undefined mechanism /existed/ when
acrolein was present in the mixture at concentrations of lesser toxic potency
that of carbon monoxide.
Incubation of isolated hepatocytes with allyl
alcohol results in GSH depletion and subsequent cytotoxicity which is prevented
by pyrazole, an inhibitor of alcohol dehydrogenase. Both GSH depletion and
cytotoxicity were much more rapid when hepatocytes were incubated with acrolein,
the reactive metabolite, and were not affected by pyrazole. However,
cytotoxicity of both allyl alcohol and acrolein was enhanced by the aldehyde
dehydrogenase inhibitors cyanamide and disulfiram. Malondialdehyde, a lipid
peroxidation product, was also formed when hepatocytes were incubated with
either agent, and treatment of hepatocytes with a ferric iron chelator,
desferrioxamine, or an antioxidant delayed the cytotoxicity without affecting
GSH depletion. ...
Pharmacology:
Interactions:
The interaction of the antihypertensive agent
guanethidine and two aldehydes possessing sympathomimetic activity on the
pressure of spontaneously hypertensive rats was studied. Acrolein (0.05-0.5
mg/kg) produced a pressor response at low doses and a depressor response at high
doses in acutely and chronically guanethidine pretreated spontaneously
hypertensive rats. Depressor responses to high doses of aldehydes may have been
attributed to vagal stimulation or direct vasodilation. There was a significant
interaction between the aldehydes and guanethidine, which may have implication
for someone undergoing treatment with guanethidine for hypertension while being
exposed to acetaldehyde and related cmpd from ethanol and tobacco smoke.
Muramyl dipeptide protection from acrolein
toxicity was tested using isolated rat hepatocytes. Incubation of hepatocyte
suspensions with acrolein (143 umol/ml) for 15 min reduced viability to 62%.
Pretreatment of hepatocytes in incubation media with muramyl dipeptide (20.6
nmol/ml) incr viability significantly to 83% p<0.05). It is suggested that
muramyl dipeptide in certain dosages may produce nonspecific stabilization of
cytoplasmic membranes towards acrolein.
The protective effect of n-acetylcysteine
against the toxicity of ... acrolein ... was investigated using isolated rat
hepatocytes as the experimental system. ... n-Acetylcysteine protected against
acrolein toxicity by providing a source of SH groups, and was effective without
prior conversion.
Groups of 30 male & 30 female Syrian
golden hamsters were exposed to 0 or 4 ppm (0 or 9.2 mg/cu m) acrolein vapor
(purity unspecified) for 7 hr/day on 5 days/wk for 52 weeks, & were given,
at the same time & also for 52 wk, weekly intratracheal instillations of 2
dose levels of benzo(a)pyrene or sc injections of n-nitrosodiethylamine (once
every 3 wk). All surviving animals were killed at 81 wk. Addnl exposure to
acrolein did not significantly incr the tumor incidence produced by
benzo(a)pyrene or N-nitrosodiethylamine.
/Male Sprague-Dawley albino/ rats were exposed
to experimental atmospheres of carbon monoxide in air, acrolein in air, and to
mixtures of carbon monoxide and acrolein in air. The toxic potency of each ...
was evaluated ... by measurement of time to incapacitation as a function of
toxic gas concentrations. ... There was no evidence of synergistic action. ...
An inhibitory or antagonistic effect of undefined mechanism /existed/ when
acrolein was present in the mixture at concentrations of lesser toxic potency
that of carbon monoxide.
Incubation of isolated hepatocytes with allyl
alcohol results in GSH depletion and subsequent cytotoxicity which is prevented
by pyrazole, an inhibitor of alcohol dehydrogenase. Both GSH depletion and
cytotoxicity were much more rapid when hepatocytes were incubated with acrolein,
the reactive metabolite, and were not affected by pyrazole. However,
cytotoxicity of both allyl alcohol and acrolein was enhanced by the aldehyde
dehydrogenase inhibitors cyanamide and disulfiram. Malondialdehyde, a lipid
peroxidation product, was also formed when hepatocytes were incubated with
either agent, and treatment of hepatocytes with a ferric iron chelator,
desferrioxamine, or an antioxidant delayed the cytotoxicity without affecting
GSH depletion. ...
Minimum Fatal Dose Level:
INHALATION OF AIR CONTAINING 10 PPM ACROLEIN
MAY BE FATAL IN A FEW MIN.
Environmental Fate & Exposure:
Environmental Fate/Exposure Summary:
Acrolein is released to the environment
through manufacturing processes and its use as an intermediate for glycerine,
methionine, glutaraldehyde and other organic chemicals. It is also released into
the environment through exhaust gas from combustion processes including tobacco
smoke, emissions from forest fires, and auto exhaust. Acrolein has also been
detected in sugar cane molasses, souring salted pork, the fish odor of cooked
horse mackerel, the volatiles from white bread, the volatile components of
chicken-breast muscle, the aroma volatiles of ripe arctic bramble berries and
the products from heating animal fats and vegetable oils. If released to air, a
vapor pressure of 274 mm Hg at 25 deg C indicates acrolein will exist solely in
the vapor-phase in the ambient atmosphere. Vapor-phase acrolein will be degraded
in the atmosphere by reaction with photochemically-produced hydroxyl radicals,
ozone, and nitrate radicals; the half-lives for these reactions in air are
estimated to be 20 hrs, 15 days, and 28 days, respectively. Acrolein in hexane
solvent show moderate absorption of UV light >290 nm, which indicated
potential for photolytic transformation under environmental conditions. If
released to soil, acrolein is expected to have very high mobility based upon an
estimated Koc of 3. Volatilization from moist soil surfaces is expected to be an
important fate process based upon a Henry's Law constant of 1.22X10-4 atm-cu
m/mole. Acrolein may volatilize from dry soil surfaces based upon its vapor
pressure. If released into water, acrolein is not expected to adsorb to
suspended solids and sediment based upon the estimated Koc. The half-life of
acrolein in natural unsterilized water was 29 hours compared with 43 hours in
sterilized (thymol-treated) water. Volatilization from water surfaces is
expected to be an important fate process based upon this compound's Henry's Law
constant. Estimated volatilization half-lives for a model river and model lake
are 4.4 hrs and 4.6 days, respectively. An estimated BCF of 3 suggests the
potential for bioconcentration in aquatic organisms is low. Hydrolysis is not
expected to occur due to the lack of hydrolyzable functional groups.
Occupational exposure to acrolein may occur through inhalation and dermal
contact with this compound at workplaces where acrolein is produced or used.
Exposure of the general population occurs primarily through atmospheric contact.
(SRC)
Probable Routes of Human Exposure:
/In a 1974 report/, acrolein was detected in a
truck-maintenance shop in USA at a mean concn of 4.6 ug/cu m. The following
exposures to acrolein in workplace air have been reported: (1) levels of
0.44-1.5 mg/cu m ... in a Russian rubber vulcanization plant producing
styrene-butadiene rubber footwear components /from a 1969 report/; (2) 0.11-1.04
mg/cu (0.04-0.4 ppm) during the welding of metals coated with anti-corrosion
primers /from a 1973 report/; (3) 0.22-0.32 mg/cu m in pitch-coking plants,
0.004-0.014 in coal-coking plants /from a 1972 report/; and (4) less than 0.1
mg/cu m (0.04 ppm) from diesel train engine exhaust during repair and servicing
/from a 1973 report/. Acrolein was found at quarries in exhaust gases from
diesel engines and in workplace air at levels of 2.1-7.2 mg/cu m /from a 1981
report/.
NIOSH (NOES Survey 1981-1983) has
statistically estimated that 65 workers are exposed to acrolein in the USA(1).
However, this estimate does not include exposure to tradename compounds which
contain acrolein. Occupational exposure to acrolein may occur through inhalation
and dermal contact with this compound at workplaces where acrolein is produced
or used(SRC). Exposure of the general population occurs primarily through
atmospheric contact(1). The variety of outdoor and indoor sources includes
incomplete combustion of fuels and other organic compounds, production and
manufacturing processes, photochemical oxidation of airborne hydrocarbons, and
cigarette smoke (both first- and secondhand)(2). Despite different sources,
typical atmospheric concentrations (1- 20 ppb) usually differ little between
indoor and outdoor air(2).
Natural Pollution Sources:
Aldehydes are reported to be common products
of a variety of microbial and vegetative processes(1). Acrolein has been
identified as a volatile component of essential oil extracted from the wood of
oak trees(2). Acrolein has been detected in sugar cane molasses, souring salted
pork, the fish odor of cooked horse mackerel, the volatiles from white bread,
the volatile components of chicken-breast muscle, the aroma volatiles of ripe
arctic bramble berries and the products from heating animal fats and vegetable
oils(2). Small amounts of acrolein have been detected in tomatoes(3) and in
chicken and beef volatiles(4).
Artificial Pollution Sources:
An estimated 46.7 tons of acrolein were
emitted into the USA atmosphere during 1978. Acrolein has been identified as an
emission from plants mfr acrylic acid. Acrolein emissions have ... been reported
from coffee-roasting operations (none detected to 0.6 mg/cu m), from a
lithographic plate coater (less than 0.23 to 3.9 mg/cu m) and from an
automobile-spray booth (1.1 to 1.6 mg/cu m). Addnl sources of atmospheric
acrolein that have been identified incl turbine engines, the mfr of fish oils,
lacquers, plastics and synthetic rubber, forest fires and spray painting.
It has been estimated that acrolein, acetone
and low-molecular-wt fatty acids are emitted at the rate of 1 million kg/year
during the mfr of oxidation-hardening enamels in the Netherlands. Acrolein was
detected in the USSR in air samples from populated areas located in the vicinity
of 3 enamelled wire mfr plants. It has ... been detected in ventilation gases
from paint and varnish preparation and distributing shops in USSR.
Acrolein was detected among other trace odors
in air in Japan: (1) in exhaust gas from a metal paint drier (6.1 mg/cu m); (2)
in exhaust gas from 2 poultry-manure dryers (3.1-4.2 mg/cu m); and (3) in
exhaust gas from a corn-starch mfr works (1.8 mg/cu m).
Acrolein is released to the environment
through manufacturing processes and its use as an intermediate for glycerine,
methionine, glutaraldehyde and other organic chemicals. It is also released into
the environment through exhaust gas from combustion processes including tobacco
smoke, emissions from forest fires, and auto exhaust. Direct application to
water and wastewater during use as an aquatic herbicide and slimicide and from
formation in the atmosphere as a photooxidation product of various hydrocarbon
pollutants including 1,3-butadiene are potential sources of acrolein in the
environment(1-5).
The main source of acrolein is incomplete
organic combustion(1). Specific point sources include residential fireplaces,
burning of coal, oil, and natural gas in power plants, automobile exhaust,
overheated vegetable and animal fats, tobacco and marijuana smoke, and
structural and vegetative fire smoke(1).
Environmental Fate:
AQUATIC FATE: EXPTL DATA FOR DECAY OF ACROLEIN
IN WATER INDICATE APPROX 1ST ORDER KINETICS. THE REACTION CONTINUED TO
COMPLETION IN NATURAL WATER. DATA ON EFFECTS OF PH ON DECAY OF ACROLEIN MAY BE
USED AS A CONSERVATIVE ESTIMATE OF DISSIPATION RATE. IN WATER FLOWING IN 2
CHANNELS, AN 8 TO 10 FOLD DISCREPANCY BETWEEN OBSERVED & PREDICTED RATES OF
DISSIPATION WAS ATTRIBUTED TO MAJOR LOSSES IN VOLATILIZATION & ADSORPTION. A
RELATIVELY NONVOLATILE REACTION PRODUCT (WHICH GAVE A POSITIVE REACTION WITH
DINITROPHENYLHYDRAZINE) ACCUMULATED INITIALLY BUT DISSIPATED.
TERRESTRIAL FATE: In the terrestrial
environment, it is estimated that acrolein would have a low tendency to adsorb
on soil and would probably volatilize into the air or be leached from the soil
by water.
AQUATIC FATE: Half-life in water at pH 5, 150
hr; at pH 7, 120-180 hr; at pH 9, 5 to 40 hr.
AQUATIC FATE: Acrolein is removed from aqueous
environments, with half-lives usually on the order of less than a day. The
primary loss process appears to be an initial hydration (and possibly some
biotransformation) to beta-hydroxypropionaldehyde, which is then further
biotransformed.
Due to its high vapor pressure and water
solubility, acrolein is expected to be highly mobile when released into the
environment, although degradative processes are likely to limit its transport.
TERRESTRIAL FATE: Based on a classification
scheme(1), an estimated Koc value of 3(SRC), determined from a structure
estimation method(2), indicates that acrolein is expected to have very high
mobility in soil(SRC). Volatilization of acrolein from moist soil surfaces is
expected to be an important fate process(SRC) given a Henry's Law constant of
1.22X10-4 atm-cu m/mole(3). The potential for volatilization of acrolein from
dry soil surfaces may exist(SRC) based upon a vapor pressure of 274 mm Hg(4).
Results of biodegradation screening studies indicate that acrolein would be
readily degraded by mixed microbial populations(5-7). The half-life of acrolein
in natural unsterilized water was 29 hours compared with 43 hours in sterilized
(thymol-treated) water(8).
AQUATIC FATE: Based on a classification
scheme(1), an estimated Koc value of 3(SRC), determined from an estimation
method(2), indicates that acrolein is not expected to adsorb to suspended solids
and sediment(SRC). Volatilization from water surfaces is expected(3) based upon
a Henry's Law constant of 1.22X10-4 atm-cu m/mole(4). Using this Henry's Law
constant and an estimation method(3), volatilization half-lives for a model
river and model lake are 4.4 hrs and 4.6 days, respectively(SRC). The decay of
acrolein and its hydration product 3- hydroxypropanal displayed first order
kinetics in agricultural canals when applied at the recommended rate for aquatic
weed control(5); the half-life for this reaction is 21 days. The dissipation
half-life of acrolein was 10.2 and 7.3 hours in weedy and non-weedy canals,
respectively. In the weedy canal, 91.5% of acrolein had dissipated within 33.0
hours and in the non-weedy canal, 48% had dissipated within 7.9 hours(5). The
half-life of acrolein in natural unsterilized water was 29 hours compared with
43 hours in sterilized (thymol-treated) water(6). In another experiment,
acrolein added to irrigation channels at initial concentrations of 6.1, 17.5 and
50.5 ppm underwent 100% loss in 12.5 days(7). Removal rate constants ranging
from 0.27-0.34 1/days were calculated by linear regression. These values
correspond to half-lives of 2.0-2.5 days(8). According to a classification
scheme(9), an estimated BCF of 3(SRC), from a log Kow of -0.01(10) and a
regression-derived equation(11), suggests the potential for bioconcentration in
aquatic organisms is low. Reaction with singlet oxygen or alkylperoxy radicals,
and photolysis are not expected to be important fate processes.
ATMOSPHERIC FATE: According to a model of
gas/particle partitioning of semivolatile organic compounds in the
atmosphere(1), acrolein, which has a vapor pressure of 274 mm Hg at 25 deg C(2),
is expected to exist solely in the vapor-phase in the ambient atmosphere.
Vapor-phase acrolein is degraded in the atmosphere by reaction with
photochemically-produced hydroxyl radicals(SRC); the half-life for this reaction
in air is estimated to be 20 hrs(SRC), calculated from its rate constant of
1.99X10-11 cu cm/molecule-sec at 25 deg C(3). Products of the reaction of
acrolein with hydroxyl radicals include: carbon dioxide, formaldehyde,
glycoaldehyde, ketene, and peroxypropenyl nitrate(4). The half-life for acrolein
reacting with ozone in the atmosphere has been estimated to be 15 days based on
an experimentally determined reaction rate constant of 7.4X10-19 cu
cm/molecule-sec at room temperature(5) and assuming an average ambient ozone
concentration of 7X10+11 molecules/cu cm(5). The half-life for acrolein reacting
with nitrate radical in the atmosphere has been estimated to be 28 days based on
an experimentally determined reaction rate constant of 1.20X10-15 cu
cm/molecule-sec at room temperature(6) and assuming an average ambient ozone
concentration of 2.4X10+8 molecules/cu cm(7). Acrolein in hexane solvent show
moderate absorption of UV light >290 nm(8), which indicated potential for
photolytic transformation under environmental conditions(SRC).
Environmental Biodegradation:
AEROBIC: The half-life of acrolein in natural
unsterilized water was 29 hours compared with 43 hours in sterilized (thymol-treated)
water(1). These results suggest that biodegradation may be partially responsible
for the degradation of acrolein in the environment. 100% loss was observed when
5 and 10 mg/l acrolein underwent a static incubation in the dark at 25 deg C
with sewage inoculum for 7 days(2). In another experiment, acrolein reached 30%
of its BOD in river water after 100 hrs(3). Results of other biodegradation
screening studies also indicate that acrolein would be readily degraded by mixed
microbial populations(4-6). In contrast, no BOD removal was observed during a
5-day BOD dilution test in which effluent from a biological waste treatment
plant was used(7).
ANAEROBIC: Acrolein, at an initial
concentration of 50 mg/l as organic carbon, gave no evidence of degradation when
incubated for 8 weeks in a 10% anaerobic sludge inoculum(1).
Environmental Abiotic Degradation:
Acrolein has been determined to be one product
of the photooxidation of 1,3-butadiene in air. This photooxidation reaction may
contribute to significant ambient atmospheric levels of acrolein because of the
occurrence of 1,3-butadiene at concn of approx 4.6 ug/cu m in urban ambient air.
Acrolein contains no functional groups which
would be suspectible to chemical hydrolysis under environmental conditions(1,2).
Arcolein will be susceptible to formation of beta-hydroxypropionaldehyde by
hydration in water. Hydration is a reversible reaction with an equilibrium
constant of 21.2. The half-life for hydration of acrolein has been calculated to
be 21 days based on a pseudo-first order reaction rate constant of 0.032
day-1(1). Half-lives for acrolein reacting with singlet oxygen and alkyl peroxy
radicals in natural sunlit water have been estimated to be 8 and 23 years,
respectively. These values are based on reaction rate constants of 1X10+7 and
3.4X10+3 l/mole-hr, respectively, a singlet oxygen concentration of 1X10-12
mole/l and an alklyl peroxy radical concentration of 1X10-9 mole/l(2). Acrolein
in hexane solvent show moderate absorption of UV light >290 nm(2), which
indicated potential for photolytic transformation under environmental
conditions(SRC). However, hydration of acrolein in water would destroy the
chromophores which absorb light. As a result, the potential for direct
photolysis would be slight(2).
The rate constant for the vapor-phase reaction
of acrolein with photochemically-produced hydroxyl radicals is 1.99X10-11 cu
cm/molecule-sec at 25 deg C(1). This corresponds to an atmospheric half-life of
approximately 20 hrs at an atmospheric concentration of 5X10+5 hydroxyl radicals
per cu cm(2). Products of the reaction of acrolein with hydroxyl radicals
include: carbon dioxide, fomaldehyde, and glycolaldhyde. In the presence of
nitrogen oxides, products include peroxyacetylnitrate and nitric acid(3). The
half-life for acrolein reacting with ozone in the atmosphere has been estimated
to be 15 days based on an experimentally determined reaction rate constant of
7.4X10-19 cu cm/molecule-sec at room temperature(4) and assuming an average
ambient ozone concentration of 7X10+11 molecules/cu cm(4). The rate constant for
the vapor-phase reaction of acrolein with nitrate radicals is 1.20X10-15 cu
cm/molecule-sec at 25 deg C(5). This corresponds to an atmospheric half-life of
approximately 28 days at an atmospheric concentration of 2.4X10+8 nitrate
radicals per cu cm(6). Based on these values, reaction with hydroxyl radical is
expected to be the most important fate process for acrolein in the ambient
atmosphere(SRC). The half-life for photodissociation of acrolein in the
atmosphere has been estimated to be approximately 3.5 days based on measured
quantum yields(7).
Environmental Bioconcentration:
A BCF of 344 has been measured for acrolein in
bluegill sunfish(1). However, this value may be an overestimate since total
(14)C was measured and may have included acrolein metabolites. An estimated BCF
of 3 was calculated for acrolein(SRC), using a log Kow of -0.01(2) and a
regression-derived equation(3). According to a classification scheme(4), this
BCF suggests the potential for bioconcentration in aquatic organisms is low.
Soil Adsorption/Mobility:
Koc = 5.0 (calculated from water solubility by
regression equations).
Using a structure estimation method based on
molecular connectivity indices(1), the Koc for acrolein can be estimated to be
3(SRC). According to a classification scheme(2), this estimated Koc value
suggests that acrolein is expected to have very high mobility in soil.
Volatilization from Water/Soil:
The Henry's Law constant for acrolein is
1.22X10-4 atm-cu m/mole(1). This Henry's Law constant indicates that acrolein is
expected to volatilize from water surfaces(2). Based on this Henry's Law
constant, the volatilization half-life from a model river (1 m deep, flowing 1
m/sec, wind velocity of 3 m/sec)(2) is estimated as 4.4 hrs(SRC). The
volatilization half-life from a model lake (1 m deep, flowing 0.05 m/sec, wind
velocity of 0.5 m/sec)(2) is estimated as 4.6 days(SRC). Acrolein's Henry's Law
constant(1) indicates that volatilization from moist soil surfaces may occur(SRC).
The potential for volatilization of acrolein from dry soil surfaces may
exist(SRC) based upon a vapor pressure of 274 mm Hg(3).
Environmental Water Concentrations:
SURFACE WATER: Acrolein concn in surface water
was reported as follows: USEPA STORET Data Base - 798 water samples, 0.25% pos.,
median concn <14 ug/l(1).
RAIN/SNOW: Levels of acetone and acrolein in
rainwater samples obtained in CA ranged from not detected-0.05 mg/l (detection
limit not reported)(1). Levels of acetone-acrolein-propanal in cloud, mist and
fog samples obtained in CA ranged from not detected-0.86 mg/l (detection limit
not reported)(1).
Effluent Concentrations:
Present in 6 out of 11 samples of municipal
effluent from Dayton, OH, concn range 20-200 ug/l(1). Detected in raw sewage in
2 sewage treatment plants in Chicago at concn ranging from 216-825 ug/l;
although concn in final effluents were below 100 ug/l(2). USEPA STORET Data Base
- 1265 effluent samples, 1.5% pos., median concn <10.0 ug/l(3). Acrolein has
been identified in emissions from: plants manufacturing acrylic acid, not
quantified; coffee roasting operations, not detected-0.6 mg/cu m (detection
limit not reported); from a lithographic plate coater, <0.23-3.9 mg/cu m; and
from an automobile spray booth, 1.1-1.6 mg/cu m(1). Detected in 1 out of 5
leachate samples from a Wisconsin municipal solid waste landfill(4).
In the Netherlands, total emissions in 1980
were estimated at 701 tons/yr from mobile sources and 31 tons/yr from stationary
sources(1). Acrolein has been detected in gasoline exhaust ranging from 0.2-5.3
ppm(2). Acrolein comprises 2.6-9.8 % volume of total gasoline exhaust aldehydes.
It has been reported that acrolein accounts for 5% of the total aldehydes
present in diluted car exhaust(2). In the United States, it is estimated that
emission of aldehydes from fireplaces is 14-54 Gg/yr; total acrolein emissions
(representing 3.5%-5.7% of total aldehydes) are roughly 0.5-3.1 Gg/yr(1).
Production loss estimates by way of fugitive emissions and equipment leakage
were 76,300 lbs in 1978(1). Tobacco and marijuana smoke represent another
significant source of atmospheric acrolein for both smokers and nonsmokers(1).
Cigarettes contribute 3-228 ug acrolein/cigarette while marijuana cigarettes
(joints) contribute 92-162 ug. The concentration of acrolein emitted from wood
furniture coatings was measured(3). Twenty days after a wood finishing product
had been applied to a piece of wood furniture, the acrolein concentration was
1280 ug/cu m(3).
Sediment/Soil Concentrations:
Acrolein was detected in sediment/soil/water
samples collected from Love Canal in Niagara Falls, NY during 1980(1). USEPA
STORET Data Base - 331 sediment samples, 0% pos.(2).
Atmospheric Concentrations:
Levels between less than 1 and 20 mg/cu m are
considered representative of concn present in urban air.
Acrolein has been found at very low concn
(0.44 to 32 ug/cu m) in ambient air in urban & suburban areas.
Air-monitoring data obtained between 1961 & 1976 show that this compound
occurred at mean ambient levels of 16 ug/cu m in Los Angeles, CA (urban
atmosphere, 42 data points) and at mean levels of 0.7 ug/cu m in Edison, NJ
(near emissions source, 19 data points).
URBAN/SUBURBAN: Air samples collected in
Claremont, CA during Aug-Sept 1979 contained acrolein at a max concn of 34 mg/cu
m(1). Acrolein accounts for about 1-13% of total atmospheric aldehydes and
occurs at approximately 8-26% of the formaldehyde concentration in urban air.
Urban air from Tokyo, Japan had an average acrolein concentration of 7.2 ppb,
while in the Netherlands mean concentrations of 0.5 ppb in ambient air have been
reported(2). Levels up to 32 ug/cu m (13.9 ppb) were measured in outdoor urban
air in Japan, Sweden, and the United States, with extremely high levels
associated within or near structural and vegetation fires(2). The average
concentration of acrolein in urban air from Los Angeles from 1961 to 1968 ranged
from 4-7 ppb with max concentrations reaching 14 ppb(3). The average
concentration of acrolein in Sao Paulo and Salvador, Brazil in 1988 was 0.56 and
0.13 ppb, respectively(3).
SOURCE DOMINATED: During June-July 1976, in
air of Edison, NJ (near emission sources), 19 samples, mean concn 0.71 ng/cu
m(1). During a 12 month period in 1968, acrolein was detected in air of the Los
Angeles Basin at levels ranging from not detected to 0.04 mg/cu m (detection
limit not reported), although most measurements were between 0.002-0.02 mg/cu
m(2). Acrolein was detected at a level of 0.14 mg/cu m in an atmospheric grab
sample obtained near an oil fire(3). Acrolein was detected at 0.057 to 0.085 ppm
(detection limit not stated) at the Portsmouth Naval Shipyard in New
Hampshire(4).
Food Survey Values:
Alcoholic beverages often contain trace
amounts of acrolein. It is sometimes a problem since it causes an organoleptic
condition called "pepper" by the alcohol fermentation industry ...
acrolein is detectable in low-proof whiskey at concn as low as 10 mg/l. This
value probably represents the upper limit for acrolein, since industry has
adapted corrective procedures to reduce "pepper" by reducing acrolein
concn.
... Acrolein is a component of many foods, and
processing can increase the acrolein content.
... Acrolein was identified in raw turkey.
Acrolein has been detected in sugar cane
molasses, souring salted pork, the fish odor of cooked horse mackerel, the
volatiles from white bread, the volatile components of chicken-breast muscle,
the aroma volatiles of ripe arctic bramble berries and the products from heating
animal fats and vegetable oils(1). This compound has also been detected in fresh
lager beer at levels of 1.11-2.00 ug/l, mean concn 1.6 ug/l(1).
Small amounts of acrolein have been detected
in tomatoes, cooked potatoes, beer, wine, rums, whiskey, and raw chicken(1).
Glycerol dehydration is a main source of acrolein in foods. Since glycerides are
the main constituent of lipids, foods containing a high fat content will be
potential sources of acrolein, principally during cooking. Significant amounts
of acrolein are produced from heated oils(1). The amount of acrolein formed from
oil heated above 300 deg C in lard, corn oil, cottonseed oil, and sunflower oil
were 109, 164, 5.1, and 163 ug/l, respectively(1). However, some oils, such as
olive, peanut, rapeseed, and sesame, can undergo auto oxidation at temperatures
as low as 80 deg C. This suggests that kitchen workers using these oils may be
exposed to acrolein since they use temperatures as high as 200 deg C(1). Olive
oil, the most unsaturated, produced the highest amounts of acrolein while
soybean oil, the most saturated, produced the lowest. Acrolein has been detected
in chicken and beef volatiles(concentrations not specified)(2).
Plant Concentrations:
... Measured the unsaturated aldehyde fraction
in raw cocoa beans and chocolate liquor. ... They measured 2-enol concn of 0.6
to 2.0 umol/100 g fat in raw cocoa beans and 1.3 to 5.3 umol/100 g in the
chocolate liquor.
No acrolein was detected 1 day following high
application rates to lettuce.
Fish/Seafood Concentrations:
Acrolein was detected in fish at the following
concn: USEPA STORET Data Base - 87 samples, 1% pos., median concn <1.0 ug/kg
wet basis(1).
Other Environmental Concentrations:
Found in: tobacco smoke, 3-141 ug/cigarette;
diesel engine exhaust gas, 0.06-19.6 mg/cu m; gasoline engine exhaust gas,
0.46-12.2 mg/cu m; rotary gasoline engine exhaust gas, 0.46 mg/cu m; combustion
products of hydraulic fluid; smoke from the combustion of wood, 115 mg/cu m,
kerosene, <2.3 mg/cu m and cotton, 138 mg/cu m; combustion products of
cellophane used to seal meat packages; and decomposition products of overheated
wax(1). Acrolein emissions from a wood burning fireplace ranged from 21-132
mg/kg of wood burned(1).
Acrolein is formed by photochemical
degradation of hydrocarbons, particularly 1,3-butadiene; the irradiation of
1,3-butadiene in the presence of NO and air gave a 55% yield(1). Acrolein may
also be produced in higher organisms as a metabolite of allylamine and allyl
alcohol, the anticancer drug cyclophosphamide, and spermine or spermidine, or
through UV irradiation of skin lipids(1).
Environmental Standards & Regulations:
FIFRA Requirements:
Classified for restricted use, limited to use
by or under the direct supervision of a certified applicator. Acrolein as sole
active ingredient in a formulation is classified as restricted for all uses
based on inhalation hazard to humans and residue effects on avian species and
aquatic organisms. No mixtures are registered.
As the federal pesticide law FIFRA directs,
EPA is conducting a comprehensive review of older pesticides to consider their
health and environmental effects and make decisions about their future use.
Under this pesticide reregistration program, EPA examines health and safety data
for pesticide active ingredients initially registered before November 1, 1984,
and determines whether they are eligible for reregistration. In addition, all
pesticides must meet the new safety standard of the Food Quality Protection Act
of 1996. Pesticides for which EPA had not issued Registration Standards prior to
the effective date of FIFRA, as amended in 1988, were divided into three lists
based upon their potential for human exposure and other factors, with List B
containing pesticides of greater concern and List D pesticides of less concern.
Acrolein is found on List B. Case No: 2005; Pesticide type: Fungicide,
herbicide, antimicribial; Case Status: OPP is reviewing data from the
pesticide's producers regarding its human health and/or environmental effects,
or OPP is determining the pesticide's eligibility for reregistration and
developing the Reregistration Eligibility Decision (RED) document.; Active
ingredient (AI): Acrolein; Data Call-in (DCI) Date(s): 05/06/91; AI Status: The
producers of the pesticide has made commitments to conduct the studies and pay
the fees required for reregistration, and are meeting those commitments in a
timely manner.
Acceptable Daily Intakes:
/The National Academy of Sciences/ estimated
the ADI for man to be 15.6 ug/kg or 1.09 mg/man, assuming a 70 kg body weight.
TSCA Requirements:
Section 8(a) of TSCA requires manufacturers of
this chemical substance to report preliminary assessment information concerned
with production, use, and exposure to EPA as cited in the preamble in 51 FR
41329.
Pursuant to section 8(d) of TSCA, EPA
promulgated a model Health and Safety Data Reporting Rule. The section 8(d)
model rule requires manufacturers, importers, and processors of listed chemical
substances and mixtures to submit to EPA copies and lists of unpublished health
and safety studies. 2-Propenal is included on this list.
CERCLA Reportable Quantities:
Persons in charge of vessels or facilities are
required to notify the National Response Center (NRC) immediately, when there is
a release of this designated hazardous substance, in an amount equal to or
greater than its reportable quantity of 1 lb or 0.454 kg. The toll free number
of the NRC is (800) 424-8802; In the Washington D.C. metropolitan area (202)
426-2675. The rule for determining when notification is required is stated in 40
CFR 302.4 (section IV. D.3.b).
Releases of CERCLA hazardous substances are
subject to the release reporting requirement of CERCLA section 103, codified at
40 CFR part 302, in addition to the requirements of 40 CFR part 355. Acrolein is
an extremely hazardous substance (EHS) subject to reporting requirements when
stored in amounts in excess of its threshold planning quantity (TPQ) of 500 lbs.
RCRA Requirements:
P003; As stipulated in 40 CFR 261.33, when
acrolein, as a commercial chemical product or manufacturing chemical
intermediate or an off-specification commercial chemical product or a
manufacturing chemical intermediate, becomes a waste, it must be managed
according to federal and/or state hazardous waste regulations. Also defined as a
hazardous waste is any container or inner liner used to hold this waste or any
residue, contaminated soil, water, or other debris resulting from the cleanup of
a spill, into water or on dry land, of this waste. Generators of small
quantities of this waste may qualify for partial exclusion from hazardous waste
regulations (40 CFR 261.5(e)).
Atmospheric Standards:
This action promulgates standards of
performance for equipment leaks of Volatile Organic Compounds (VOC) in the
Synthetic Organic Chemical Manufacturing Industry (SOCMI). The intended effect
of these standards is to require all newly constructed, modified, and
reconstructed SOCMI process units to use the best demonstrated system of
continuous emission reduction for equipment leaks of VOC, considering costs, non
air quality health and environmental impact and energy requirements. Acrolein is
produced, as an intermediate or a final product, by process units covered under
this subpart.
Listed as a hazardous air pollutant (HAP)
generally known or suspected to cause serious health problems. The Clean Air
Act, as amended in 1990, directs EPA to set standards requiring major sources to
sharply reduce routine emissions of toxic pollutants. EPA is required to
establish and phase in specific performance based standards for all air emission
sources that emit one or more of the listed pollutants. Acrolein is included on
this list.
Clean Water Act Requirements:
Toxic pollutant designated pursuant to section
307(a)(1) of the Federal Water Pollution Control Act and is subject to effluent
limitations.
Acrolein is designated as a hazardous
substance under section 311(b)(2)(A) of the Federal Water Pollution Control Act
and further regulated by the Clean Water Act Amendments of 1977 and 1978. These
regulations apply to discharges of this substance. This designation includes any
isomers and hydrates, as well as any solutions and mixtures containing this
substance.
State Drinking Water Guidelines:
(AZ) ARIZONA 320 ug/l
(FL) FLORIDA 110 ug/l
FDA Requirements:
Food starch may be esterified and etherified
by treatment with one of the following: Acrolein, not to exceed 0.6% and vinyl
acetate, not to exceed 7.5%. Limitations: Acetyl groups in food starch-modified
not to exceed 2.5%.
Food starch may be etherified by treatment
with one of the following: Acrolein, not to exceed 0.6%.
Chemical/Physical Properties:
Molecular Formula:
C3-H4-O
Molecular Weight:
56.06
Color/Form:
Colorless or yellowish liquid
Colorless or yellow liquid ...
Odor:
Extremely sharp; extremely acrid, pungent,
burnt sweet; hot fat
... Piercing, disagreeable odor.
Boiling Point:
52.5 deg C @ 760 mm Hg
Melting Point:
-88 deg C
Corrosivity:
Non-corrosive to iron & steel at room
temperature
Density/Specific Gravity:
0.8389 @ 20 deg C; 0.8621 @ 0 deg C; 0.8075 @
50 deg C
Heat of Combustion:
-12,500 BTU/lb= -6,950 cal/g= -290X10+5 J/kg
Heat of Vaporization:
216 BTU/lb= 120 cal/g= 5.02X10+5 J/kg
Octanol/Water Partition Coefficient:
log Kow= -0.01
pH:
pH 6.0 (max); a 10% solution in water at 25
deg C.
Solubilities:
SOL IN PETROLEUM ETHER
Sol in alc, ether
Soluble in oxygenated solvents
Miscible with lower alcohols, ketones,
benzene, diethyl ether ...
In water, 208 g/kg @ 20 deg C
In water, 2.12X10+5 mg/l @ 25 deg C
Spectral Properties:
Index of refraction: 1.4022 @ 19 deg C/D
INDEX OF REFRACTION: 1.4017 @ 20 DEG C/D
SADTLER REF NUMBER: 6645 (IR, PRISM)
MAX ABSORPTION (ETHYL ALCOHOL): 207 NM (LOG E
= 4.05)
Acrolein has a moderate UV absorption in the
solar spectral region. For acrolein in hexane, the extinction coefficients at
wavelengths of 303 nm, 328 nm, 336 nm, 360 nm, and 386 nm, are 9.7 M-1 cm-1,
18.5 M-1 cm-1, 21.0 M-1 cm-1, 13.5 M-1 cm-1, and 5.0 M-1 cm-1, respectively.
IR: 6646 (Sadtler Research Laboratories Prism
Collection)
UV: 5-8 (Organic Electronic Spectral Data,
Phillips et al, John Wiley & Sons, New York)
NMR: 9153 (Sadtler Research Laboratories
Spectral Collection)
MASS: 22 (Atlas of Mass Spectral Data, John
Wiley & Sons, New York)
Surface Tension:
24 DYNES/CM = 0.024 N/M AT 20 DEG C
Vapor Density:
1.94 (Air= 1)
Vapor Pressure:
274 mm Hg @ 25 deg C
Viscosity:
0.35 cP @ 20 deg C
Other Chemical/Physical Properties:
Conversion factors: 1 mg/l = 437 ppm; 1 ppm =
2.3 mg/cu m
HEAT OF POLYMERIZATION: -50 BTU/LB = -28 CAL/G
= -1.2X10+5 J/KG (EST); LIQ-WATER INTERFACIAL TENSION: 35 DYNES/CM = 0.035 N/M @
20 DEG C (EST); RATIO OF SPECIFIC HEATS OF VAPOR (GAS): 1.1487
BP: 17.5 deg C @ 200 mm Hg; 2.5 deg C @ 100 mm
Hg; -7.5 deg C @ 60 mm Hg; -64.5 deg C @ 1.0 mm Hg
VP: 210 MM HG @ 20 DEG C; 135.71 MM HG @ 10
DEG C; 325.70 MM HG @ 30 DEG C; 692.15 MM HG @ 50 DEG C
Unstable, polymerizes (especially under light
or in the presence of alkali or strong acid) forming diacryl, a plastic solid.
Henry's Law constant= 1.22X10-4 atm-cu m/mol @
25 deg C
Hydroxyl radical rate constant= 1.22X10-11 cu
cm/molecule-sec @ 25 deg C
Chemical Safety & Handling:
DOT Emergency Guidelines:
Health: Toxic; may be fatal if inhaled,
ingested or absorbed through skin. Inhalation or contact with some of these
materials will irritate or burn skin and eyes. Fire will produce irritating,
corrosive and/or toxic gases. Vapors may cause dizziness or suffocation. Runoff
from fire control or dilution water may cause pollution. /Acrolein, inhibited/
Fire or explosion: Highly flammable: Will be
easily ignited by heat, sparks or flames. Vapors may form explosive mixtures
with air. Vapors may travel to source of ignition and flash back. Most vapors
are heavier than air. They will spread along ground and collect in low or
confined areas (sewers, basements, tanks). Vapor explosion and poison hazard
indoors, outdoors or in sewers. Some may polymerize (P) explosively when heated
or involved in a fire. Runoff to sewer may create fire or explosion hazard.
Containers may explode when heated. Many liquids are lighter than water. /Acrolein,
inhibited/
Public safety: Call Emergency Response
Telephone Number. ... Isolate spill or leak area immediately for at least 100 to
200 meters (330 to 660 feet) in all directions. Keep unauthorized personnel
away. Stay upwind. Keep out of low areas. Ventilate closed spaces before
entering. /Acrolein, inhibited/
Protective clothing: Wear positive pressure
self-contained breathing apparatus (SCBA). Wear chemical protective clothing
which is specifically recommended by the manufacturer. It may provide little or
no thermal protection. Structural firefighters' protective clothing is
recommended for fire situations only; it is not effective in spill situations. /Acrolein,
inhibited/
Evacuation: ... Fire: If tank, rail car or
tank truck is involved in a fire, isolate for 800 meters (1/2 mile) in all
directions; also, consider initial evacuation for 800 meters (1/2 mile) in all
directions. /Acrolein, inhibited/
Fire: CAUTION: All these products have a very
low flash point. Use of water spray when fighting fire may be inefficient. Small
fires: Dry chemical, CO2, water spray or alcohol-resistant foam. Large fires:
Water spray, fog or alcohol-resistant foam. Move containers from fire area if
you can do it without risk. Dike fire control water for later disposal; do not
scatter the material. Do not use straight streams. Fire involving tanks or
car/trailer loads: Fight fire from maximum distance or use unmanned hose holders
or monitor nozzles. Cool containers with flooding quantities of water until well
after fire is out. Withdraw immediately in case of rising sound from venting
safety devices or discoloration of tank. ALWAYS stay away from the ends of
tanks. For massive fire use unmanned hose holders or monitor nozzles; if this is
impossible, withdraw from area and let fire burn. /Acrolein, inhibited/
Spill or leak: Fully encapsulating, vapor
protective clothing should be worn for spills and leaks with no fire. ELIMINATE
all ignition sources (no smoking, flares, sparks or flames in immediate area).
All equipment used when handling the product must be grounded. Do not touch or
walk through spilled material. Stop leak if you can do it without risk. Prevent
entry into waterways, sewers, basements or confined areas. A vapor suppressing
foam may be used to reduce vapors. Small spills: Absorb with earth, sand or
other non-combustible material and transfer to containers for later disposal.
Use clean non-sparking tools to collect absorbed material. Large spills: Dike
far ahead of liquid spill for later disposal. Water spray may reduce vapor; but
may not prevent ignition in closed spaces. /Acrolein, inhibited/
First aid: Move victim to fresh air. Call
emergency medical care. Apply artificial respiration if victim is not breathing.
Do not use mouth-to-mouth method if victim ingested or inhaled the substance;
induce artificial respiration with the aid of a pocket mask equipped with a
one-way valve or other proper respiratory medical device. Administer oxygen if
breathing is difficult. Remove and isolate contaminated clothing and shoes. In
case of contact with substance, immediately flush skin or eyes with running
water for at least 20 minutes. Wash skin with soap and water. Keep victim warm
and quiet. Effects of exposure (inhalation, ingestion or skin contact) to
substance may be delayed. Ensure that medical personnel are aware of the
material(s) involved, and take precautions to protect themselves. /Acrolein,
inhibited/
Odor Threshold:
0.21 PPM /PURITY NOT SPECIFIED/
Air: 0.16 ul/l; Water: 0.11 mg/l; Odor safety
class D; D= 10-50% of attentive persons can detect TLV concn in the air
Low= 0.0525 mg/cu m; High= 37.5000 mg/cu m;
Irritating concn= 1.25 mg/cu m.
Skin, Eye and Respiratory Irritations:
Acrolein produces intense irritation to the
eye and mucous membranes of the respiratory tract.
Intense lacrimation & nasal irritation ...
The general sequence of acrolein irritation is
concentration-time dependent eg, 1 ppm for 1 min gives slight nasal irritation;
1 ppm for 5 min gives intolerable eye irritation; 5.5 ppm for 5 seconds gives
moderate eye irritation; & 5.5 ppm for 1 min produces marked lacrimation.
...
Severe irritation of the eyes, skin, mucous
membranes; ... .
Acrolein is intensely irritating to the eyes
... . ... Skin irritation ... can be produced from prolonged or repeated
contact.
Fire Potential:
Flammable liquid
NFPA Hazard Classification:
Health: 4. 4= Materials that, on very short
exposure, could cause death or major residual injury, including those that are
too dangerous to be approached without specialized protective equipment. A few
whiffs of the vapor or gas can cause death, or contact with the vapor or liquid
may be fatal, if it penetrates the fire fighter's normal protective gear. The
normal full protective clothing and breathing apparatus available to the typical
fire fighter will not provide adequate protection against inhalation or skin
contact with these materials.
Flammability: 3. 3= This degree includes Class
IB and IC flammable liquids and materials that can be easily ignited under
almost all normal temperature conditions. Water may be ineffective in
controlling or extinguishing fires in such materials.
Reactivity: 3. 3= This degree includes
materials that, in themselves, are capable of detonation, explosive
decomposition, or explosive reaction, but require a strong initiating source or
heating under confinement. This includes materials that are sensitive to thermal
and mechanical shock at elevated temperatures and pressures and materials that
react explosively with water. Fires involving these materials should be fought
from a protected location.
Flammable Limits:
Lower flammable limit: 2.8% by volume; Upper
flammable limit: 31% by volume
Flash Point:
-15 DEG F (CLOSED CUP); -26 DEG C (CLOSED CUP)
LESS THAN 0 DEG F (OPEN CUP); -18 DEG C (OPEN
CUP)
Autoignition Temperature:
428 DEG F (220 DEG C) UNSTABLE
Fire Fighting Procedures:
Fire fighting procedure: In advanced or
massive fires, fire fighting should be done from a safe distance, or from a
protected location. Use dry chemical, alcohol foam, or carbon dioxide. water may
be ineffective but water should be used to keep fire exposed containers cool. If
a leak or spill has not ignited, use water spray to disperse vapors. If it is
necessary to stop a leak, use water spray to protect personnel attempting to do
so. Water spray may be used to flush spills away from exposures and to dilute
spills to nonflammable mixtures. Acrolein vapors are uninhibited and may form
polymers in vents or flame arrestors of storage tanks, resulting in stoppage of
vents.
If material on fire or involved in fire: Do
not extinguish fire unless flow can be stopped. Use water in flooding quantities
as fog. Solid streams of water may be ineffective. Cool all affected containers
with flooding quantities of water. Apply water from as far a distance as
possible. Use "alcohol" foam dry chemical or carbon dioxide. /Acrolein,
inhibited/
Evacuation: If fire becomes uncontrollable or
container is exposed to direct flame, consider evacuation of one mile radius. /Acrolein,
inhibited/
The high toxicity & volatility of acrolein
require use of air packs or air breathing equipment for any significant /fire
involving acrolein/.
Use water spray, dry chemical, "alcohol
resistant" foam, or carbon dioxide. Use water spray to keep fire-exposed
containers cool. Approach fire from upwind to avoid hazardous vapors and toxic
decomposition products. Fight fire from protected location or maximum possible
distance. /Acrolein, inhibited/
Toxic Combustion Products:
Toxic gases and vapors (such as carbon
monoxide and peroxides) may be released in a fire involving acrolein.
Firefighting Hazards:
VAPOR IS HEAVIER THAN AIR ... & MAY TRAVEL
A CONSIDERABLE DISTANCE TO A SOURCE OF IGNITION & FLASH BACK.
Explosive Limits & Potential:
LOWER 2.8%; UPPER 31%
Hazardous Reactivities & Incompatibilities:
Mixing acrolein and oleum in a closed
container caused the temperature and pressure to increase.
Mixing acrolein and oleum in a closed
container caused the temperature and pressure to increase.
Mixing acrolein and 70% nitric acid in a
closed container caused the temperature and pressure to increase.
Mixing acrolein and ethyleneimine in a closed
container caused the temperature and pressure to increase.
Mixing acrolein and chlorosulfonic acid in a
closed container caused the temperature and pressure to increase.
Mixing acrolein and 28% ammonium hydroxide in
a closed container caused the temperature and pressure to increase.
Mixing acrolein and 2-aminoethanol in a closed
container caused the temperature and pressure to increase.
In the presence of alkaline or strong acid
contamination, which acts as a catalyst, acrolein undergoes a condensation
reaction liberating around 300 kJ/kg acrolein reacted. This reaction may be very
rapid & violent.
Water initiates exothermic reactions catalyzed
by mineral acids & possibly some metallic salts. An interference between
acrolein & water appears to promote the reaction & it is not prevented
by the usual acrolein polymerization inhibitors, eg, hydroquinone or
4-methoxyphenol. The reaction can be avoided by scrupulously eliminating ionic
contaminants & water layers, & maintaining reasonably low temp. To
dispose of acrolein or arrest a runaway reaction, 20 or more volumes of water
must be added to completely solubilize the acrolein ... .
Oxidizers, acids, alkalis, ammonia, amines
[Note: polymerizes readily unless inhibited -- usually with hydroquinone. May
form shock sensitive peroxides overtime].
Hazardous Decomposition:
DANGEROUS; WHEN HEATED TO DECOMPOSITION, EMITS
HIGHLY TOXIC FUMES ...
Hazardous Polymerization:
Polymerizes (especially under light or in the
presence of alkali or strong acid) forming disacryl, a plastic solid.
POLYMERIZES SLOWLY IN PRESENCE OF AIR
Acrylaldehyde is very reactive and will
polymerize rapidly, accelerating to violence, in contact with strong acid or
basic catalysts.
A 2 yr old sample stored in a refrigerator
close to a bottle of dimethylamine exploded violently, presumably after
absorbing enough volatile amine (which penetrates plastics closures) to initiate
polymerization.
May polymerize in the presence of light and
explosively in the presence of concentrated acids forming disacryl, a white
plastic solid.
Acrolein polymerizes with release of heat on
contact with minor amounts of acids (including sulfur dioxide), alkalis,
volatile amines, salts, thiourea, oxidants (air) and on exposure to light and
heat.
Immediately Dangerous to Life or Health:
2 ppm
Protective Equipment & Clothing:
CHEMICAL SAFETY GOGGLES & FACE SHIELD;
SELF-CONTAINED BREATHING APPARATUS, POSITIVE-PRESSURE HOSE MASK, AIRLINE MASK OR
INDUSTRIAL CANISTER-TYPE GAS MASK; RUBBER SAFETY SHOES; CLOTHING MADE OF RUBBER
OR OTHER IMPERVIOUS MATERIAL.
Recommendations for respirator selection. Max
concn for use: 2 ppm. Respirator Class(es): Any supplied-air respirator operated
in a continuous flow mode. May require eye protection. Any powered,
air-purifying respirator with organic vapor cartridge(s). May require eye
protection. Any chemical cartridge respirator with a full facepiece and organic
vapor cartridge(s). Any air-purifying, full-facepiece respirator (gas mask) with
a chin-style, front- or back-mounted organic vapor canister. Any self-contained
breathing apparatus with a full facepiece. Any supplied-air respirator with a
full facepiece.
Recommendations for respirator selection.
Condition: Emergency or planned entry into unknown concn or IDLH conditions:
Respirator Class(es): Any self-contained breathing apparatus that has a full
facepiece and is operated in a pressure-demand or other positive pressure mode.
Any supplied-air respirator that has a full facepiece and is operated in
pressure-demand or other positive pressure mode in combination with an auxiliary
self-contained breathing apparatus operated in pressure-demand or other positive
pressure mode.
Recommendations for respirator selection.
Condition: Escape from suddenly occurring respiratory hazards: Respirator
Class(es): Any air-purifying, full-facepiece respirator (gas mask) with a
chin-style, front- or back-mounted organic vapor canister. Any appropriate
escape-type, self-contained breathing apparatus.
Facilities for quickly drenching the body
should be provided within the immediate work area for emergency use where there
is a possibility of exposure. [Note: It is intended that these facilities
provide a sufficient quantity or flow of water to quickly remove the substance
from any body areas likely to be exposed. The actual determination of what
constitutes an adequate quick drench facility depends on the specific
circumstances. In certain instances, a deluge shower should be readily
available, whereas in others, the availability of water from a sink or hose
could be considered adequate.]
Eyewash fountains should be provided in areas
where there is any possibility that workers could be exposed to the substance;
this is irrespective of the recommendation involving the wearing of eye
protection.
Wear appropriate eye protection to prevent eye
contact.
Wear appropriate personal protective clothing
to prevent skin contact.
Preventive Measures:
WHEREVER POSSIBLE, ACROLEIN SHOULD BE STORED,
HANDLED & PROCESSED IN THE OPEN OR IN ROOFED AREAS WITH OPEN SIDES. ...
PROCESSING EQUIPMENT SHOULD BE OF TOTALLY ENCLOSED TYPE WITH AN OXYGEN-FREE
ATMOSPHERE. WHERE ACROLEIN IS HANDLED, EXHAUST &/OR GENERAL VENTILATION
SHOULD BE FITTED. ... BEFORE A TANK HAVING CONTAINED ACROLEIN IS ENTERED, IT
SHOULD BE PURGED WITH NITROGEN /VENTILATED WITH AIR/ & PRECAUTIONS RELEVANT
TO ENTERING CONFINED SPACES SHOULD BE OBSERVED.
All tanks, processing vessels, pumps,
reactors, heat exchangers, & similar equipment should be protected by
adequate emergency vent-relief devices. Acrolein vapors are not inhibited &
can form polymers in vent lines, valves, & flame arresters with subsequent
stoppage of the vent.
In case of /acrolein/ contamination with
mineral acids or alkalis, depending on the amt involved, the temp rise may be
slow enough to permit control injection of a buffer solution /of acetic acid,
glacial or hydroquinone, photo-grade or sodium acetate, anhydrous/. An emergency
supply should be available at all times in areas where acrolein is handled. The
effectiveness of stored buffer is unchanged by discoloration.
Hazardous situations are most likely to occur
when it is necessary to deviate from standard operating procedures. The acrolein
system should be a dedicated system & almost completely isolated, so that
the possibility of contamination can only occur when temporary tie-ins are made.
No hoses or lines should be used in blowing lines, washing equipment ... unless
the past history of the hose is known & the hose is thoroughly cleaned.
Contact lenses should not be worn when working
with this chemical.
SRP: The scientific literature for the use of
contact lenses in industry is conflicting. The benefit or detrimental effects of
wearing contact lenses depend not only upon the substance, but also on factors
including the form of the substance, characteristics and duration of the
exposure, the uses of other eye protection equipment, and the hygiene of the
lenses. However, there may be individual substances whose irritating or
corrosive properties are such that the wearing of contact lenses would be
harmful to the eye. In those specific cases, contact lenses should not be worn.
In any event, the usual eye protection equipment should be worn even when
contact lenses are in place.
SRP: Contaminated protective clothing should
be segregated in such a manner so that there is no direct personal contact by
personnel who handle, dispose, or clean the clothing. Quality assurance to
ascertain the completeness of the cleaning procedures should be implemented
before the decontaminated protective clothing is returned for reuse by the
workers. Contaminated clothing should not be taken home at end of shift, but
should remain at employee's place of work for cleaning.
Air packs or fresh air breathing masks should
be available in an area where acrolein is handled. Safety showers & eye
baths must be avail in the area.
Evacuation: If material leaking (not on fire),
consider evacuation from downwind area based on amount of material spilled,
location and weather conditions. /Acrolein, inhibited/
Personnel protection: Avoid breathing vapors.
Keep upwind. ... Avoid bodily contact with the material. ... Do not handle
broken packages without protective equipment. Wash away any material which may
have contacted the body with copious amounts of water or soap and water. /Acrolein,
inhibited/
If material not on fire and not involved in
fire: Keep sparks, flames, and other sources of ignition away. Keep material out
of water sources and sewers. Build dikes to contain flow as necessary. Attempt
to stop leak if without undue personnel hazard. Use water spray to disperse
vapors and dilute standing pools of liquid. /Acrolein, inhibited/
Eating and smoking should not be permitted in
areas where liquid acrolein is handled, processed, or stored.
The worker should immediately wash the skin
when it becomes contaminated.
Work clothing that becomes wet should be
immediately removed due to its flammability hazard.
Stability/Shelf Life:
UNSTABLE
The stability of acrolein is very dependent on
pH.
Shipment Methods and Regulations:
No person may /transport,/ offer or accept a
hazardous material for transportation in commerce unless that person is
registered in conformance ... and the hazardous material is properly classed,
described, packaged, marked, labeled, and in condition for shipment as required
or authorized by ... /the hazardous materials regulations (49 CFR 171-177)./
The International Air Transport Association (IATA)
Dangerous Goods Regulations are published by the IATA Dangerous Goods Board
pursuant to IATA Resolutions 618 and 619 and constitute a manual of industry
carrier regulations to be followed by all IATA Member airlines when transporting
hazardous materials.
The International Maritime Dangerous Goods
Code lays down basic principles for transporting hazardous chemicals. Detailed
recommendations for individual substances and a number of recommendations for
good practice are included in the classes dealing with such substances. A
general index of technical names has also been compiled. This index should
always be consulted when attempting to locate the appropriate procedures to be
used when shipping any substance or article.
Storage Conditions:
Separate from oxidizing materials, peroxides,
acids, and alkalies. Store in a cool, dry, well-ventilated location, protected
from sunlight. Outside or detached storage is preferred. Inside storage should
be in a standard flammable liquids storage warehouse, room, or cabinet. Do not
store uninhibited acrolein.
For storage, the pH of acrolein is adjusted to
5-6 by the addition of acetic acid.
... Can be stored under oxygen-free nitrogen
in dark glass bottles, in cylinders, or in black iron drums.
Should be handled in a fume hood or closed
system with exhaust ventilation of adequate scrubbing facilities. Should be
stored in air-tight containers with nitrogen gas filled in a cool,
well-ventilated place away from sources of possible ignition or fire. Do not
store uninhibited acrolein under any circumstances. When filled drums or other
containers are stored in separate storage rooms, trapped door drains should be
provided and floors pitched to the drains. The storage areas should be provided
with automatic sprinkler or other adequate extinguishing system. Acids, alkalis
or oxidants should not be stored nearby. Outdoors or isolated storage place is
preferable.
Cleanup Methods:
1. Remove all ignition sources. 2. Ventilate
the area of spill or leak. 3. for small quantities, absorb on paper towels.
evaporate in safe place (such as fume hood). Allow sufficient time for
evaporating vapors to completely clear hood ductwork. Burn paper in suitable
location away from combustible materials. For large quantities, cover with
sodium bisulfite add small amount of water, and mix. Then, after 1 hr, flush
with large amt of water, and wash site with soap solution. Liquid should not be
allowed to enter confined space, such as sewer, because of possibility of
explosion.
Environmental considerations: Land spill: Dig
a pit, pond, lagoon, or holding area to contain liquid or solid material. /SRP:
If time permits, pits, ponds, lagoons, soak holes, or holding areas should be
sealed with an impermeable flexible membrane liner./ Dike surface flow using
soil, sand bags, foamed polyur or foamed concrete. Neutralize with sodium
bisulfate. /Acrolein, inhibited/
Environmental considerations: Air spill: Apply
water or mist to knock down vapors. Combustion products include corrosive or
toxic vapors. /Acrolein, inhibited/
Environmental considerations: Water spill: Use
natural barriers or oil spill control booms to limit spill motion. Add sodium
bisulfate. If dissolved, apply activated carbon at ten times the spilled amount.
Use mechanical dredges or lifts to remove immobilized masses of pollutants and
precipitates. /Acrolein, inhibited/
Spills of liquid acrolein are handled by
covering the acrolein with 6 inches of National 99 Aero-O-Foam to suppress
evaporation; Polymerization of the spilled acrolein by adding a dilute, 5-10%
aqueous sodium carbonate solution should then be ... /applied/. Dilute aqueous
sodium bisulfite may be used on small spills.
Releases may require isolation or evacuation.
Eliminate all ignition sources. Use water spray to cool and disperse vapors,
protect personnel, and dilute spills to form nonflammable mixtures. /Acrolein,
inhibited/
Disposal Methods:
Generators of waste (equal to or greater than
100 kg/mo) containing this contaminant, EPA hazardous waste number P003, must
conform with USEPA regulations in storage, transportation, treatment and
disposal of waste.
Aqueous wastes with low concn of acrolein are
usually neutralized with sodium hydroxide and fed to a sewage treatment plant
for biological secondary treatment. Concentrated wastes are reprocessed whenever
possible or burned in special waste incinerators. Recommendable methods:
Neutralization, incineration. Not recommendable methods: Discharge to sewer,
landfill. Peer-review: Old acrolein may be explosive as a result of very fast
self-polymerization reaction. Handle with care. Dissolve in water, add excess
10% sodium bisulfate soln. ... (Peer-review conclusions of an IRPTC expert
consultation (May 1985))
Incineration: Dissolve in a combustible
solvent, then spray the soln into the furnace with afterburner.
Acrolein is a waste chemical stream
constituent which may be subject to ultimate disposal by controlled
incineration. (1500 deg F, 0.5 sec minimum for primary combustion; 2000 deg F,
1.0 sec for secondary combustion)
A good candidate for liquid injection
incineration at a temperature range of 650 to 1,600 deg C and a residence time
of 0.1 to 2 seconds. A good candidate for rotary kiln incineration at a
temperature range of 820 to 1,600 deg C and residence times of seconds for
liquids and gases, and hours for solids. A good candidate for fluidized bed
incineration at a temperature range of 450 to 980 deg C and residence times of
seconds for liquids and gases, and longer for solids.
Group I Containers: Combustible containers
from organic or metallo-organic pesticides (except organic mercury, lead,
cadmium, or arsenic compounds) should be disposed of in pesticide incinerators
or in specified landfill sites. /Organic or metallo-organic pesticides/
Group II Containers: Non-combustible
containers from organic or metallo-organic pesticides (except organic mercury,
lead, cadmium, or arsenic compounds) must first be triple-rinsed. Containers
that are in good condition may be returned to the manufacturer or formulator of
the pesticide product, or to a drum reconditioner for reuse with the same type
of pesticide product, if such reuse is legal under Department of Transportation
regulations (eg 49 CFR 173.28). Containers that are not to be reused should be
punctured ... and transported to a scrap metal facility for recycling, disposal
or burial in a designated landfill. /Organic or metallo-organic pesticides/
The following wastewater treatment
technologies have been investigated for acrolein: Biological treatment.
The following wastewater treatment
technologies have been investigated for acrolein: Activated carbon.
Occupational Exposure Standards:
OSHA Standards:
Permissible Exposure Limit: Table Z-1 8-hr
Time Weighted Avg: 0.1 ppm (0.25 mg/cu m).
Vacated 1989 OSHA PEL TWA 0.1 ppm (0.25 mg/cu
m); STEL 0.3 ppm (0.8 mg/cu m) is still enforced in some states.
Threshold Limit Values:
Ceiling limit: 0.1 ppm, skin
A4. A4= Not classifiable as a human
carcinogen.
NIOSH Recommendations:
Recommended Exposure Limit: 10 Hr
Time-Weighted Avg: 0.1 ppm (0.25 mg/cu m).
Recommended Exposure Limit: 15 Min Short-Term
Exposure Limit: 0.3 ppm (0.8 mg/cu m).
Immediately Dangerous to Life or Health:
2 ppm
Other Occupational Permissible Levels:
USSR (1966): 0.3 ppm; Czechoslavakia (1969):
0.2 ppm.
Emergency Response Planning Guidelines (ERPG):
ERPG(1) 0.1 ppm (no more than mild, transient effects) for up to 1 hr exposure;
ERPG(2) 0.5 ppm (without serious, adverse effects) for up to 1 hr exposure;
ERPG(3) 3 ppm (not life threatening) up to 1 hr exposure.
Manufacturing/Use Information:
Major Uses:
For Acrolein (USEPA/OPP PC Code: 000701)
active products with label matches. /SRP: Registered for use in the U.S. but
approved pesticide uses may change periodically and so federal, state and local
authorities must be consulted for currently approved uses./
Mfr colloidal forms of metals; making
plastics, perfumes; warning agent in methyl chloride refrigerant; has been used
in military poison gas mixtures. Used in organic synthesis. Aquatic herbicide.
CHEMICAL INT IN SYNTH OF GLYCERIN, ... ACRYLIC
ACID, & ESTERS; PESTICIDE
Intermediate for glycerol, polyurethane,
polyester resins, and pharmaceuticals
Aquatic herbicide, rodenticide
Applied to control the growth of aquatic weeds
in irrigation waterways or of algae and mollusks in recirculating water systems.
FOR CONTROL OF SUBMERGED WEEDS (POTAMOGETON,
NAJAS, ZANNICHELLIA, CERATOPHYLLUM, SPIROGYRA, & OTHERS) & FLOATING
WEEDS (WATER CRESS, WATER HYACINTH & WATER PRIMROSE) IN IRRIGATION CANALS,
DITCHES. ... ALSO AN ALGICIDE.
Used as a liquid fuel
Chemical intermediate for DL-methionine, its
hydroxy analog, and their salts; as a microbiocide in oil wells; Used to make
modified food starch
Direct uses of acrolein are as a tissue
fixative, which when coupled with a freeze substitution technique is valuable
for preserving enzyme activity in histochemical investigations, a leather
tanning agent, and recently, in tests, as a fumigant for ground squirrel
burrows.
In world War I, it was used as a tear gas
under the name Papite.
Cellulose fibre crosslinking agent
It is used in the manufacture of
pharmaceuticals, perfumes, food supplements, and resins. It is also used as a
biocide and fungicide.
Manufacturers:
Union Carbide Corporation, Hq, Old Ridgebury
Road, Danbury, CT 06817; (203) 794-2000; Production site: Taft, LA 70057
Degussa-Huls Corp., 65 Challenger Rd.,
Ridgefield Park, NJ 07660, (201)641-6100; Chemical Group; Production site:
Theodore, AL 36590
Methods of Manufacturing:
It was produced commercially starting in 1938
by the vapor-phase condensation of acetaldehyde & formaldehyde. In 1959, the
direct oxidation of propylene in presence of a catalyst became the preferred
commercial process, & variations of this process are the only methods
currently used commercially. The acetaldehyde-formaldehyde route was last used
in the USA in 1970.
Prepared ... by passing glycerol vapors over
magnesium sulfate heated to 330-340 deg C.
... /Oxidation of/ propylene with
bismuth-phosphorus-molybdenum catalyst.
Lab prepn by heating mixt of anhydrous
glycerol, acid potassium sulfate and potassium sulfate in presence of ...
hydroquinone and distilling in dark.
General Manufacturing Information:
IT WAS INTRODUCED AS AN AQUATIC HERBICIDE
& ALGICIDE BY THE SHELL CHEMICAL CO UNDER THE TRADE NAME "AQUALIN"
OR "AQUALINE" (A NAME NO LONGER USED FOR THIS PRODUCT IN SOME
COUNTRIES) & PROTECTED BY US PATENTS 2,042,220; 2,959,476; 2,978,475.
AQUALIN /HAS BEEN/ ... DISCONTINUED BY SHELL
CHEMICAL CO.
The commercial production of acrolein started
in Japan in 1960. Three Japanese companies currently mfr it for sale ... one of
these companies & three others produce acrolein as an intermediate in the
synthesis of acrylic acid & its esters.
NOT PHYTOTOXIC TO COMMON FIELD CROPS WHEN USED
AS DIRECTED BY PRODUCT LABEL.
Formation from glycerol by the action of B.
amaracrylus: Boisenet, Compt. Rend. 199, 941, 1271 (1929)
The commercial product contains a
polymerization inhibitor such as hydroquinone. When used as a reagent in fine
chemical applications, acrolein is usually produced in situ from acetaldehyde
and aqueous formaldehyde.
Must be stored in the dark, under nitrogen.
Method of Purification: Rectification
Formulations/Preparations:
USEPA/OPP PC Code 000701; Trade Names: Aqualin,
Crolean, Magnacide H, Acquinite, NSC 8819.
MAGNACIDE H LIQUID HERBICIDE--92% ACROLEIN.
AQUALINE HERBICIDE (SHELL)--85% ACROLEIN.
Grade: Technical.
Acrolein is available in the USA as a
commercial grade with minimum purity of 92% & contains 0.1-0.25%
hydroquinone as an inhibitor.
Technical grade is 92-97%.
Impurities:
Impurities include water, 4.0% max, &
small amounts of acetaldehyde & propionaldehyde.
Propionaldehyde and acetone are the principal
carbonyl impurities in freshly distilled acrolein.
Consumption Patterns:
The largest market for acrolein is for
methionine manufacture (1978)
In the production of D,L-methionine by Rhone-Poulenc
in France, approximately 2,000 tons/annually of acrolein are produced and
consumed.
More than 80% of the refined acrolein that is
produced today goes into the synthesis of methionine. Much larger quantities of
crude acrolein are produced as an intermediate in the production of acrylic
acid. More than 85% of the acrylic acid produced worldwide is by the captive
oxidation of acrolein.
In Australia, over 66 tons were used annually
for control of submersed plants in more than 4000 km of irrigation canals.
U. S. Production:
(1972) 2.72X10+10 G
(1974) 2.77X10+10 G
(1991) 900 million lb
U. S. Imports:
(1972) NEGLIGIBLE
U. S. Exports:
(1972) NEGLIGIBLE
Laboratory Methods:
Clinical Laboratory Methods:
An accurate and sensitive high-performance
liquid chromatographic method is described for estimation of acrolein at 1 ng
level in biological tissues (kidney and liver) using a ultra violet detector.
The method was based on the reaction of acrolein with
2,4-dinitrophenylhydrazine. The recovery of the acrolein-1,2-dinitrophenyl-
hydrazine adduct from tissue homogenates under simulated conditions by 3
different methods was fair to poor (5-44%). The recovered material consistently
had shorter retention times than acrolein standards.
Fluorescence spectroscopy has been used to
determine the acrolein present in biological systems.
Analytic Laboratory Methods:
NIOSH Method 2539. Analyte: Acrolein.
Procedure: Gas chromatography, flame ionization detector and gas
chromatography/mass spectrometry. For acrolein this method has an estimated
detection limit of 2 ug aldehyde/sample. The precision/RSD is not determined.
Applicability: This is a screening technique to determine the presence of
aldehydes and should not be used for quantitation. Interferences: High boiling
naphtha mixtures, may have components with retention times similar to the
acrolein and may be interferences in the gas chromatographic analysis.
NIOSH Method 2501. Analyte: Acrolein.
Procedure: Gas chromatography, nitrogen-specific detector. For acrolein this
method has an estimated detection limit of 2 ug/sample. The precision/RSD is not
determined. Applicability: The method has sufficient sensitivity for personnal
monitoring below the PEL of 0.1 ppm with an 8 hr sample collected at 0.01 l/min.
Interferences: None known.
Acrolein has been ... determined as its
2,4-dinitrophenylhydrazone derivative using gas chromatography with
flame-ionization detection in (1) diesel automobile engine exhaust; (2)
automobile engine exhaust; & (3) the aroma volatiles of ripe arctic bramble
berries, using thin-layer & gas chromatography with mass spectrometry
confirmation. Gas chromatography with flame-ionization detection has also been
used to determine the content of acrolein in waste-water, with a limit of
detection of 0.5 mg/l. ... A microwave spectrophotometric method has been used
to determine acrolein in automobile exhaust.
Acrolein in air (0.13-1.5 mg/cu m) reacted
with 10% (wt/wt) 2-(hydroxymethyl)piperidine coated on XAD-2 (16/50 mesh)
sorbent to produce a bicyclic oxazolidine,
9-vinyl-1-aza-8-oxabicyclo(4.3.0)nonane. This cmpd was desorbed from the sorbent
with toluene and determined by gas chromatography with nitrogen-specific
detection.
Differential Pulse Polarography is used to
determine acrolein in natural water. Prepare sample by buffering with phosphate;
add ethylenediaminetetraacetic acid. Range of detection is 0.05 to 0.5 mg/l.
Liquid Chromatography/Electrochemistry is used
to determine acrolein in aqueous solution. Prepare sample by derivatizing with
2,4-dinitrophenylhydrazine. Limit of detection is 99 pg.
High Pressure Liquid Chromatography equipped
with flame ionization detector is used to determine acrolein in automobile
exhaust. Sample is prepared by diluting & then bubbling through impingers
containing 2-diphenylacetyl-1,3-indandione-1-hydrazone in acetonitrile &
hydrochloric acid catalyst. Limit of detection is 1.4 ug/cu m (20 l samples).
High pressure liquid chromatography equipped with ultraviolet detection has a
detection limit of 11 ug/cu m (20 liter samples).
NIOSH Method: 211. Analyte: Acrolein. Matrix:
Air. Procedure: Colorimetry. Method Evaluation: Method was validated over the
range of 1 to 30 ug/10 ml using a 50 l sample. Precision (CVt): + or - 5% for
standards, unknown for air samples. Interferences: There is no interferences
from sulfur dioxide, nitrogen dioxide, ozone and most organic air pollutants. A
slight interference occurs from dienes: 1.5% for 1,3-butadiene and 2% for
1,3-pentadiene.
EPA Method 8030. Gas Chromatographic analysis
of acrolein, acrylonitrile, and acetronitrile. Detection is achieved by a flame
ionization detector. For acrolein the method detection limit is 0.7 ug/l, the
average recovery range for four samples is 42.9 to 60.1 ug/l, and the limit for
the standard deviation is 4.6 ug/l.
EPA Method 8240. Gas Chromatography/Mass
Spectrometry for the determination of volatile Organics. This method can be used
to quantify most volatile organic compounds including acrolein that have boiling
points below 200 deg C and are insoluble or slightly soluble in water. The
detection limit is not given. Precision and method accuracy were found to be
directly related to the concentration of the analyte and essentially independent
of the sample matrix.
EPA Method 603. Purge-and-Trap Gas
Chromatography Method with electrolytic conductivity detection for the
determination of acrolein and acrylonitrile in municipal and industrial
discharges. Under the prescribed conditions for acrolein the method has a
detection limit of 0.7 ug/l and an average recovery of 9.3 ug/l for industrial
water at a spike concentration of 100 ug/l.
NIOSH Method 5031. Detection of Volatile,
Nonpurgeable, Water-Soluble Compounds by Azeotropic Distillation.
NIOSH Method 8316. Determination of Acrylamide,
Acrylonitrile and Acrolein by High Performance Liquid Chromatography (HPLC).
NIOSH Method 8315. Determination of Carbonyl
Compounds by High Performance Liquid Chromatography (HPLC).
Sampling Procedures:
A personal air sampling method for acrolein
has been developed based on the use of the solid sorbent Amberlite XAO-2 coated
with 2,4-dinitrophenyl-hydrazine. Using this method, acrolein in the range of
0.02-0.52 ppm can be analyzed in 5 liter samples with a recovery of 80-100%.
Personal air sampling method: Use of
hydroquinone-treated carbon as the solid sorbent.
A personal air sampling method /for acrolein
has been developed/ using a Porapak N adsorption tube to trap acrolein with
subsequent thermal desorption. With this method, acrolein concentrations below 1
ppm can be determined with recovery efficiencies approaching 100%.
NIOSH Method 2539. Analyte: Acrolein. Sampler:
Solid sorbent tube (10% 2-(hydroxymethyl)piperidine on XAD-2, 120 mg/60 mg).
Flow Rate: 0.01 to 0.05 l/min: Sample Size: 5 liters. Shipment: @ 25 deg C or
lower. Sample Stability: Stable greater or equal to 1 week @ 25 deg C.
NIOSH Method 2501. Analyte: Acrolein. Sampler:
Solid sorbent tube 2-(hydroxymethyl)piperidine on XAD-2, 120 mg/60 mg. Flow
Rate: 0.01 to 0.1 l/min: Sample Size: 48 liters. Shipment: Routine. Sample
Stability: At least 4 weeks @ 25 deg C.
NIOSH Method 211. Analyte: Acrolein. Matrix:
Air. Procedure: Collection in midget impinger with 1% aqueous sodium sulfite,
reaction with 4-hexyl resorcinol. Flow Rate: 2.0 l/min. Sample Size: 50 liters.
Special References:
Special Reports:
GENERAL REVIEW OF ACROLEIN & OTHER
ALDEHYDES IS FOUND IN FORMALDEHYDE & OTHER ALDEHYDES, NAS/NRC (1981).
FOLMAR LC; ACROLEIN, DALAPON, DICHLOBENIL,
DIQUAT, AND ENDOTHAL: BIBLIOGRAPHY OF TOXICITY TO AQUATIC ORGANISMS; US FISH
WILD L SERV TECH PAP (88): 1-16 (1977). TOXICITY TABLES LIST TEST ORGANISMS
(PLANTS, INVERTEBRATES & o VERTEBRATES), TYPES OF TESTS, EXPTL CONDITIONS
& TEST RESULTS FOR ACROLEIN & OTHER CHEMICALS. EACH TABLE IS FOLLOWED BY
REFERENCES.
Toxicology Review: Environmental Health
Perspectives, DHEW Publication 11: 163 (1975)
Toxicology Review: Cahiers de Medecine du
Travail 10 (3): 49 (1973)
Toxicology Review: Mutation Research 47: 115
(1977)
USEPA; Chemical Hazard Information Profile:
Acrolein (1980) EPA 560/11-80-011
USEPA; Ambient Water Quality Criteria Doc:
Acrolein (1980) EPA 440/5-80-016
DHHS/ATSDR; Toxicological Profile for Acrolein
(1990) ATSDR/TP-90/01, NTIS PB91-180307
WHO; Environmental Health Criteria 127:
Acrolein (1992)
USEPA/ECAO; Ambient Water Quality Criteria
Document: Addendum for Acrolein. Final Draft (9/89) ECAO Pub. ECAO-CIN-614
Synonyms and Identifiers:
Synonyms:
Acquinite
**PEER REVIEWED**
ACRALDEHYDE
**PEER REVIEWED**
ACROLEINA (ITALIAN)
**PEER REVIEWED**
ACROLEINE (DUTCH, FRENCH)
**PEER REVIEWED**
ACRYLALDEHYDE
**PEER REVIEWED**
ACRYLALDEHYD (GERMAN)
**PEER REVIEWED**
ACRYLIC ALDEHYDE
**PEER REVIEWED**
AI3-24160
**PEER REVIEWED**
AKROLEINA (POLISH)
**PEER REVIEWED**
AKROLEIN (CZECH)
**PEER REVIEWED**
ALDEHYDE ACRYLIQUE (FRENCH)
**PEER REVIEWED**
ALDEIDE ACRILICA (ITALIAN)
**PEER REVIEWED**
Allyl aldehyde
**PEER REVIEWED**
Caswell No 009
**PEER REVIEWED**
Crolean
**PEER REVIEWED**
EPA Pesticide Chemical Code 000701
**PEER REVIEWED**
NSC 8819
**PEER REVIEWED**
Papite
**PEER REVIEWED**
PROPENAL
**PEER REVIEWED**
2-PROPENAL
**PEER REVIEWED**
PROP-2-EN-1-AL
**PEER REVIEWED**
PROPENAL (CZECH)
**PEER REVIEWED**
2-PROPEN-1-ONE
**PEER REVIEWED**
Formulations/Preparations:
USEPA/OPP PC Code 000701; Trade Names: Aqualin,
Crolean, Magnacide H, Acquinite, NSC 8819.
MAGNACIDE H LIQUID HERBICIDE--92% ACROLEIN.
AQUALINE HERBICIDE (SHELL)--85% ACROLEIN.
Grade: Technical.
Acrolein is available in the USA as a
commercial grade with minimum purity of 92% & contains 0.1-0.25%
hydroquinone as an inhibitor.
Technical grade is 92-97%.
Shipping Name/ Number DOT/UN/NA/IMO:
UN 1092; Acrolein, inhibited
IMO 3.1; Acrolein, inhibited
Standard Transportation Number:
49 064 10; Acrolein, inhibited
EPA Hazardous Waste Number:
P003; An acute hazardous waste when a
discarded commercial chemical product or manufacturing chemical intermediate or
an off-specification commercial chemical product or a manufacturing chemical
intermediate.
RTECS Number:
NIOSH/AS1050000
Administrative Information:
Hazardous Substances Databank Number: 177
Last Revision Date: 20020213
Last Review Date: Reviewed by SRP on 9/14/2000