effects of DDM exposure

Chuck Miller rellim at MAILHOST.TCS.TULANE.EDU
Thu Jun 4 15:59:15 EST 1998

Hi Chris and others,

Below are a few selected recent articles and abstracts on DDM toxicity.

Try a Medline search for the information--it's free.


Best of results,


Dr. Charles A. Miller, III,   rellim at mailhost.tcs.tulane.edu
Dept. Environmental Health Sciences, SL29
Tulane-Xavier Center for Bioenvironmental Research and
Tulane Univ. School of Public Health and Tropical Medicine
1430 Tulane Ave.
New Orleans, LA 70112
(504)585-6942, fax (504)584-1726
Bionet.toxicology newsgroup: http://www.bio.net/hypermail/TOXICOLOGY

Am J Pathol 1997 Oct;151(4):905-909

Bile ductular damage induced by methylene dianiline
inhibits oval cell activation.

Petersen BE, Zajac VF, Michalopoulos GK

Department of Pathology, University of Pittsburgh, Pennsylvania 15261, USA.

Administration of 2-acetylaminofluorene (2-AAF) given before a two-thirds
partial hepatectomy (PHx),
results in suppression of hepatocyte proliferation and stimulation of oval
cell proliferation. Our objective
in this study was to examine the oval cell response and associated
alpha-fetoprotein (AFP) gene
expression by combining 2-AAF with selective hepatic damage caused by
either carbon tetrachloride
(CCl4) exposure or by PHx. We also examined oval cell response with the
above two protocols
(2-AAF/CCl4 and 2-AAF/PHx) as affected by previous bile ductular damage
caused by 4,4'-methylene
dianiline (4,4'-diaminodiphenylmethane, DAPM) exposure. DAPM is an aromatic
diamine, known to
cause bile ductular damage in both humans and animals. Using the protocols
of 2-AAF/ CCl4 and
2-AAF/PHx, when DAPM was given 24 hours before the hepatic injury, no oval
cell proliferation was
seen (histological) and AFP expression was not detected by Northern blot
analysis. These results
provide direct evidence that oval cells are closely associated with the
biliary epithelial cells and supports
the theory that hepatic oval cells may originate from cells derived from
either intraportal or periportal

PMID: 9327722, UI: 97468657

Toxicology 1997 Oct 19;122(3):193-204

Modulation of taurine levels in the rat liver alters
methylene dianiline hepatotoxicity.

Seabra V, Timbrell JA

Department of Toxicology, School of Pharmacy, University of London, UK.

Methylene dianiline (DAPM) causes hepatic damage and bile duct necrosis in
rats. This has been detected
histologically and biochemically. The toxicity was dose related over the
range 0-100 mg/kg but the dose
response relationship showed a maximum at about 75-100 mg/kg. This was true
for both histopathology
and biochemical parameters of liver dysfunction. When animals were depleted
of taurine using
beta-alanine pretreatment, the toxicity of DAPM was increased. Conversely
treatment of rats with
taurine, significantly attenuated the rise in alanine transaminase (ALT).
However depletion of taurine
with guanidinoethanesulphonate (GES) attenuated rises in both
transaminases. It is concluded that
taurine may play a role in the toxicity of DAPM but that GES, although
depleting taurine as does
beta-alanine, causes additional effects such as increasing glutathione
(GSH), perhaps leading to

PMID: 9328219, UI: 97466879

Am Ind Hyg Assoc J 1997 Aug;58(8):587-591

Workers exposed to thermal degradation products of TDI-
and MDI-based polyurethane: biomonitoring of 2,4-TDA,
2,6-TDA, and 4,4'-MDA in hydrolyzed urine and plasma.

Dalene M, Skarping G, Lind P

Department of Occupational and Environmental Medicine, University Hospital,
Lund, Sweden.

The aim of the study was to investigate biomarkers of exposure to thermal
degradation products of 2,4-
and 2,6-toluene diisocyanate (TDI)- and 4,4'-methylenediphenyl diisocyanate
(MDI)-based polyurethane
and the toxicokinetics of these products. Blood and urine were collected
from 15 factory workers
exposed to thermal degradation products of MDI-based polyurethane glue and
TDI-based flexible foam.
Four of these workers were also studied during an exposure-free period.
Urine and plasma were
analyzed after acidic hydrolysis and the concentrations of the isocyanates'
corresponding amines, 2,4-,
2,6-toluenediamine (TDA), and 4,4'-methylenedianiline (MDA), were
determined as derivatives of
pentafluoropropionic anhydride by gas chromatography using chemical
ionization mass spectrometry
monitoring negative ions. Urinary elimination rates were in the range of <
0.01-5.7 micrograms of
2,4-TDA per hour, < 0.01-3.5 micrograms of 2,6-TDA per hour, and < 0.01-1.6
micrograms of
4,4'-MDA per hour. Plasma levels were in the range of < 0.1-5.5 ng of
2,4-TDA per mL, < 0.1-2.3 ng
of 2,6-TDA per mL, and < 0.1-45 ng of 4,4'-MDA per mL. The urinary
half-lives of 4,4'-MDA for four
of the workers were found to be 59, 61, 73, and 82 hours. The half-lives of
4,4'-MDA in plasma were
10, 14, 16, and 22 days. Elimination rate peaks of 2,4-TDA, 2,6-TDA, and
4,4'-MDA in urine varied
during and between workdays. The individual variation in plasma
concentrations of 2,4-TDA, 2,6-TDA,
and 4,4'-MDA with time was small, but between individuals the variation was

PMID: 9248033, UI: 97391226

Am J Contact Dermat 1997 Jun;8(2):121-124

Results of patch testing with a specialized collection of
plastic and glue allergens.

Holness DL, Nethercottdagger JR

Department of Occupational and Environmental Health, St Michael's Hospital,
University of Toronto,
Toronto, Ontario, Canada.

Patch testing was performed on 235 patients with a specialized collection
of plastic and glue
components. Thirteen percent had a positive response to at least one of the
allergens. Seventy-four
percent of the responses were relevant to either the present or a past
problem, and 64% were
occupationally related. The substances that yielded the greater percentage
of positive responses were
ethylenediamine, triethylenetetramine, diethylenetriamine,
diaminodiphenylmethane, melamine
formaldehyde resin, phenol formaldehyde resin, cresylglycidylether,
phenylglycidylether, and N,
N-dimethyl-p-toluidine. Of the 47 agents used, 26 did not elicit any
positive responses. There were few
distinguishing characteristics between those who exhibited a positive
response to these agents and those
who did not. In 12 cases (5% of those tested), the diagnosis of allergic
contact dermatitis would have
been missed if the plastics and glues components were not used.

PMID: 9171151, UI: 97298210

J Toxicol Clin Toxicol 1997;35(1):35-40

Accidental intoxication with methylene dianiline
p,p'-diaminodiphenylmethane: acute liver damage after
presumed ecstasy consumption.

Tillmann HL, van Pelt FN, Martz W, Luecke T, Welp H, Dorries F, Veuskens A,
Fischer M, Manns MP

Medizinische Hochschule Hannover, Germany.

BACKGROUND: MDA is the abbreviation for methylene dianiline (p,p'
4,4'-methylenedianiline; CAS 101-77-9); and for methylendioxyamphetamine
alpha-dimethyl-1,3-benzodioxole-5-ethanamine; CAS 42542-10-9). While the
former is used for the
production of polyurethane foams, the latter is a psychometric drug, which
is becoming increasingly
popular in the techno scene. METHODS: We report six participants of a
technoparty (1 female, 5 males,
ages 17-25) who were admitted to the hospital with severe colicky abdominal
pain and subsequently
developed symptoms of hepatotoxicity. They had ingested an alcoholic
beverage that had been spiked
with a powdery substance they dubbed MDA. RESULTS: All patients showed
similar clinical
symptoms, with an identical time course. Acute jaundice developed within 2
days after ingestion.
Enzymes indicating cholestasis increased steadily over 7 days and reached
peak values of 800 U/L (AP)
and 380 U/L (GGT), whereas transaminases remained moderately elevated.
Between days 5 and 7, all
patients became febrile for one day, their body temperatures rising up to
40 degrees C. There was no
evidence for hemolysis or an infectious hepatitis. Toxicological analysis
revealed the presence of
p,p'-diaminodiphenylmethane (4,4'-methylenedianiline) at a concentration of
130 mg/L in one of two
urine extracts examined. CONCLUSIONS: The analytical data indicate that the
participants of the
technoparty assumed the aniline-derivative, the cause of Epping Jaundice, was
methylendioxyamphetamine because the same abbreviation, MDA, is used for
both compounds. An
overview of the acute liver toxicity of aniline derivatives is given and
the possibility of
amphetamine-induced liver damage is discussed.

PMID: 9022650, UI: 97174990

Int J Dermatol 1996 Dec;35(12):852-856

Occupational allergic contact dermatitis caused by
2,4,6-tris-(dimethylaminomethyl)phenol, and review of
sensitizing epoxy resin hardeners.

Kanerva L, Estlander T, Jolanki R

Section of Dermatology, Finnish Institute of Occupational Health, Helsinki,

BACKGROUND: Epoxy resin compounds (ERC) include a large number of
sensitizing chemicals such
as epoxy resins (ER), hardeners (curing agents), and reactive diluents.
Allergic contact dermatitis (ACD)
caused by ERCS is often occupational. MATERIALS AND METHODS: We report a
patient, sensitized
to a hardener of a two-component epoxy paint. Three conventional patch test
sessions were performed to
diagnose the causative chemical. We also review the literature on
sensitizing epoxy-resin hardeners.
RESULTS: A 47-year-old nonatopic woman developed dermatitis from a
two-component epoxy paint.
Patch testing with epoxy resin was negative, but
2,4,6-tris(dimethylaminomethyl)phenol (tris-DMP),
used in the paint hardener, induced an allergic patch test reaction. We
also review briefly other epoxy
hardeners that have caused allergic dermatitis, including: (1) aliphatic
polyamines, e.g., ethylenediamine,
diethylenetriamine, triethylenetetramine, 3-dimethylaminopropylamine, and
trimethylhexamethylenediamine; (2) cycloaliphatic polyamines, e.g.,
isophoronediamine and
3,3'-dimethyl-4,4-diaminodicyclohexylmethane; (3) aromatic amines, such as
4,4'-diaminodiphenylmethane, m-phenylene diamine, and 1,3-xylylene diamine;
(4) dicyanodiamide; (5)
triglycidyl isocyanurate, an epoxy compound that may be used as an
epoxy-resin hardener; and (6)
additives in epoxy accelerators, such as hexavalent chromate. CONCLUSIONS:
No one chemical can be
used to screen for sensitization to the many different epoxy hardeners.
Extensive patch testing may be
required to reveal the hardener that has caused the allergy. The hardener,
2,4,6-tris-(dimethylaminomethyl)phenol (tris-DMP), is a new sensitizer. To
verify ACD caused by
tris-DMP, patch-testing at 1% in petrolatum is suggested.

PMID: 8970840, UI: 97125768

Chem Res Toxicol 1996 Oct;9(7):1103-1112

Synthesis and quantification of DNA adducts of

Schutze D, Sagelsdorff P, Sepai O, Sabbioni G

Institut fur Pharmakologie und Toxikologie, Universitat Wurzburg, Germany.

4,4'-Methylenedianiline (MDA) is used as a hardener in the manufacture of
plastics and polyurethanes.
MDA has been classified as a carcinogen in animals and is a suspected human
carcinogen. Assuming that
MDA would yield similar DNA adducts to other arylamines, we synthesized the
following C-8 guanine
adducts: N'-acetyl-N-(deoxyguanosin-8-yl)-MDA, N-(deoxyguanosin-8-yl)-MDA,
N-(deoxyguanosin-8-yl)-4MA, and their corresponding 3'-monophosphate
derivatives. We developed
methods to identify these adducts of MDA in liver DNA using
32P-postlabeling, HPLC, and GC-MS
techniques. Liver DNA was obtained from rats treated with radiolabeled MDA
(1.11 and 116.5
mumol/kg body weight). The total radioactivity bound to the DNA
corresponded to 0.06 and 2.7 adducts
per 10(7) nucleotides [covalent binding index (CBI = (mumol of adduct per
mol of nucleotide)/(mmol of
compound per kg body weight)) of 1.05 and 2.3]. This DNA-binding potency is
in the range of weakly
genotoxic compounds. The liver DNA was analyzed for the presence of the
synthesized adducts by the
following methods: (I) HPLC analysis of nucleotides and purines after
enzymatic and acid hydrolysis,
and (II) 32P-postlabeling after enzymatic hydrolysis. The major adducts
found in vivo did not
correspond to the synthesized standards. Further work was carried out to
determine the structure of the
unidentified adducts. It was possible to release MDA and MDA-d4 from DNA of
rats dosed with MDA
and/or MDA-d4 and from the synthesized adducts using strong base
hydrolysis. Liver of two female
Wistar rats given 500 mumol/kg MDA-2HCl was hydrolyzed in 0.1 M NaOH
overnight at 110 degrees
C. GC-MS analysis of the heptafluorobutyric anhydride derivatized
dichloromethane extracts detected
428 +/- 40 fmol of MDA/mg of DNA. In the control animals no MDA was found.
The experiment was
repeated with livers from animals dosed 500 mumol/kg MDA-d4.2DCl. In these
rats 488 +/- 19 fmol
MDA-d4 was found to be bound at liver DNA. Taking into account a 68% yield
of the method, the CBI
found in these cases was 0.82 and 1.0, respectively.

PMID: 8902264, UI: 97057934

Carcinogenesis 1996 May;17(5):1069-1073

32P-postlabeling of a DNA adduct derived from
4,4'-methylenedianiline, in the olfactory epithelium of rats
exposed by inhalation to 4,4'-methylenediphenyl

Vock EH, Hoymann HG, Heinrich U, Lutz WK

Institute of Toxicology, Swiss Federal Institute of Technology,
Schwerzenbach, Switzerland.

Tissues obtained from female Wistar rats exposed to a 0.9 microm aerosol of
diisocyanate (MDI) for 17 h per day, 5 days per week, for one year, at
levels of 0, 0.3, 0.7 and 2.0
mg/m(3), were analyzed for DNA adducts. A 32P-postlabeling method was used
to detect (i), adducts
formed by the reaction of the isocyanate group(s) of MDI with DNA; and a
32P-postlabeling method
was adapted to detect (ii), a DNA adduct formed by 4,4'- methylenedianiline
(MDA), a
hydrolysis/decarboxylation product of MDIV. In the lung, neither isocyanate
adducts nor the arylamine
adduct were detectable. The same negative result was seen in the liver, the
bladder, the kidney, the
respiratory epithelium and in peripheral lymphocytes. In the olfactory
epithelium, on the other hand, the
arylamine-derived DNA adduct was detected, at the very low levels of 5,9
and 10 adduct-nucleotides per
10(10) nucleotides, for the three dose groups, respectively. The adduct
co-chromatographed with the
one formed in the liver of rats after oral gavage of MDA. The results are
discussed in terms of the
importance of genotoxic versus nongenotoxic aspects of carcinogenesis.

PMID: 8640915, UI: 96217830

Int Arch Occup Environ Health 1996;68(3):165-169

MDA in plasma as a biomarker of exposure to pyrolysed
MDI-based polyurethane: correlations with estimated
cumulative dose and genotype for N-acetylation.

Dalene M, Jakobsson K, Rannug A, Skarping G, Hagmar L

Department of Occupational and Environmental Medicine, Lund University
Hospital, Sweden.

The object of this study was to investigate whether exposure of pipe-layers
to thermal degradation
products of diphenylmethane diisocyanate (MDI) could be assessed by
analysing 4,4-methylenedianiline
(MDA) in hydrolysed plasma and urine, and whether the genotype for
N-acetylation affected these
biomarker levels. Blood and urine samples were drawn from 30-pipe-layers
who had been welding
polyurethane (PUR) insulated pipes during the preceding 3 months. MDA in
hydrolysed plasma and
urine was determined with a gas chromatography-mass spectrometry technique,
and genotype for
N-acetylation was analysed with a polymerase chain reaction technique. MDA
in plasma was detected in
18 of the 30 pipe-layers. Their plasma concentrations of MDA varied from
0.05 to 8.48 micrograms/l.
There was a significant negative correlation between time since last
welding of PUR-insulated pipes and
P-MDA (rs = 0.50, P = 0.005). There was also a significant positive
correlation between the estimated
number of welded PUR-insulated pipes during the preceding 3 months and
P-MDA (rs = 0.68, P = <
0.001). No significant association between genotype of N-acetylation and
P-MDA was observed in a
multiple regression analysis when adjustment was made for the estimated
cumulative exposure to thermal
degradation products of MDI. MDA in urine was detected in only four of the
30 pipe-layers. These four
subjects had been welding PUR pipes on the same day as the sampling, or on
the day before. The
present results indicate the spot plasma samples analysed for MDA may give
a rather good estimate of
exposure to MDI during the preceding months. P-MDA, but not U-MDA,
therefore seems to be a useful
biomarker of long-term exposure to MDI. The individual N-acetylation
capacity did not affect the plasma
levels of MDA.

PMID: 8919844, UI: 97077277

Chem Biol Interact 1995 Jul 14;97(2):185-198

Hemoglobin adducts and urine metabolites of
4,4'-methylenedianiline after 4,4'-methylenediphenyl
diisocyanate exposure of rats.

Sepai O, Schutze D, Heinrich U, Hoymann HG, Henschler D, Sabbioni G

Institut fur Pharmakologie und Toxikologie, Universitat Wurzburg, Germany.

4,4'-Methylenediphenyl diisocyanate (MDI) is a very important component in
the production of
polyurethane. In a long-term experiment, designed to determine the
carcinogenic and toxic effects of
MDI, rats were exposed chronically for 3 and 12 months, to 0.0 (control),
0.26, 0.70 and 2.06 mg
MDI/m3 as aerosols. Hemoglobin adducts and urine metabolites of MDI were
determined at the different
doses in order to develop methods to biomonitor workers exposed to MDI and
to assess a risk resulting
from such exposure. Hemoglobin adducts and urine metabolites of
4,4'-methylenedianiline (MDA) were
found in all rats, including controls. MDA and N-acetyl-MDA (AcMDA) were
quantified by GC-MS
after derivatization with heptafluorobutyric anhydride. The dose-response
relationships for hemoglobin
adducts and urine metabolites were non-linear over this dose range. In
urine, free AcMDA and MDA
were found after base extraction. The amount of MDA present in urine and to
a lesser extent the AcMDA
found in urine correlate well with the corresponding amount determined as
hemoglobin adducts for all
dose groups. In order to release MDA from possible conjugates of MDA and
AcMDA, urine was treated
under strong acidic conditions. Following this procedure higher MDA levels
were found than the sum of
MDA and AcMDA from mild base hydrolysis. Similar results were obtained with
the rats exposed for 3
and 12 months, indicating that a steady state had been reached by 3 months.
In order to perform further
investigations of the bronchoalveolar lavage fluid one group of animals was
given a 1 week recovery
period before sacrifice. Hemoglobin adducts from these animals showed a
decrease of approximately
40% for all dose groups. According to the lifetime of rat erythrocytes the
levels of hemoglobin adducts
should have decreased by only 22%. This suggests that the erythrocytes with
modified hemoglobin have
a shorter lifespan. In order to exclude the possibility that hemoglobin
adducts may have resulted from
ingestion of hydrolyzed MDI via licking of the fur, a single dose
experiment with rats exposed through
the nose only or with the whole body was carried out. The only difference
observed between these two
exposure regimes was that the hemoglobin adduct levels of AcMDA after nose
only exposure were
significantly higher than after total body exposure. The presence of AcMDA
in urine and as a
hemoglobin adduct indicates that MDA was bioavailable after MDI exposure.
The presence of MDA may
contribute significantly to the carciongenic potential of MDI, since MDA
has been shown to be
carcinogenic in animals.

PMID: 7606816, UI: 95330849

Toxicol Lett 1995 Jul;78(2):165-171

Infusion of bile from methylene dianiline-treated rats into
the common bile duct injures biliary epithelial cells of
recipient rats.

Kanz MF, Wang A, Campbell GA

Department of Pathology, University of Texas Medical Branch, Galveston
77555-0605, USA.

Methylene dianiline (4,4'-diaminodiphenylmethane, DAPM) rapidly causes
cholestasis and injury to
biliary epithelial cells (BEC) in the liver and common bile duct of rats.
Our objective was to determine if
the proximate toxicant(s) was present in bile. Bile from DAPM-treated or
control rats was infused
through the common bile duct of untreated rats via inflow and outflow
cannulas for 4 h. Cholestasis,
increases in serum constituents, and intrahepatic BEC injury in the livers
of DAPM-treated donor rats at
4 h were comparable to previous studies (Kanz et al., Toxicol. Appl.
Pharmacol. 117 (1992) 88-97).
BEC injury in the common bile duct of rats receiving DAPM bile or control
bile was assessed by point
counting. Percent necrosis was > 28% in the common bile duct of rats
receiving DAPM bile compared to
< 5% in rats receiving control bile. These results indicate that bile is a
major route of BEC exposure to
DAPM proximate toxicant(s) and demonstrate the utility of a new method for
investigating mechanisms
of biliary toxicants.

PMID: 7618181, UI: 95343448

J Biomater Appl 1995 Jul;10(1):23-58

Formation and elution of toxic compounds from sterilized
medical products: methylenedianiline formation in

Shintani H

National Institute of Health Sciences, Department of Medical Devices,
Tokyo, Japan.

The formation of a toxic and carcinogenic compound, methylenedianiline
(MDA), in sterilized medical
use polyurethane (PU) is discussed. Due to good biocompatibility and
biostability, PU is widely used
for blood-containing devices. There are two types of PU currently available
for medical use. One is
chain-extended thermoplastic PU, the other is thermosetting PU used for
potting material connecting
fibers and modules in artificial dialyzers and plasma separators. Both
gamma-ray irradiation and
autoclave sterilization are predominantly used for the sterilization of
these devices. MDA formation in
sterilized PUs by gamma-ray irradiation and by autoclave treatment is
compared. The Delany clause in
the USA prohibits the manufacture of medical devices producing any toxic
compound during fabrication
and sterilization, therefore, the formation and elution of MDA and other
toxic compounds should be
seriously considered. Although MDA formation at a concentration of a few to
a few hundred ppb in
autoclaved chain-extended thermoplastic PU has been reported, there have
been no papers describing
MDA formation in autoclaved thermosetting PU potting material, or
describing MDA formation in
gamma-ray irradiated chain-extended thermoplastic PU and thermosetting PU.
We elected to determine
whether MDA was in fact produced in Pus sterilized by gamma-ray irradiation
or by autoclave
sterilization. Our objective was to estimate the risk factor to the human
patients or recipient. Our
conclusion is to confirm which sterilization of gamma-ray or autoclave is
more appropriate. No
formation of MDA was observed in autoclaved thermosetting PU potting
material at 121 degrees C for
60 min. A few ppm of MDA was formed in irradiated potting material. MDA
formation increased with
increasing irradiation doses. MDA formed in irradiated potting material at
2.5 Mrad (less than one ppm)
is not a significant risk to the recipient. The estimated cancer causing
risk factor when absorbing one mg
MDA/kg body weight/day is 0.29. Twenty-nine persons per 100 persons exhibit
a cancer potential.
More importantly, our experimental evidence indicated that serum extracts
from irradiated potting
material contained unknown compounds other than MDA. The presence of these
compounds is
considerably more significant and toxic. When tested, these compounds
proved to be mutagenic in the
absence of metabolic activity, thus promoting a need to identify and study
further. Compounds
indicating mutagenicity increased with increasing irradiation. Small
amounts of mutagenic compounds
were determined in extract from autoclaved potting material, smaller than
that by gamma-ray irradiation.
Therefore, autoclave sterilization is more appropriate, providing materials
can withstand the process.

PMID: 7473051, UI: 96020417

Fundam Appl Toxicol 1995 Jun;26(1):91-98

Decontamination procedures after in vitro topical exposure
of human and rat skin to 4,4'-methylenebis[2-chloroaniline]
and 4,4'-methylenedianiline.

Hewitt PG, Hotchkiss SA, Caldwell J

Department of Pharmacology and Toxicology, St. Mary's Hospital Medical
School, Imperial College of
Science, Technology and Medicine, London, United Kingdom.

4,4'-Methylenebis[2-chloroaniline] (MbOCA) and 4,4'-methylenedianiline
(MDA) are widely used
industrial chemicals classified as suspect human carcinogens. There is
considerable occupational skin
exposure to these compounds, and consequently, it is important to establish
an efficient washing
procedure after skin contamination. Four washing solutions were studied
(100% ethanol, 100% water, 1
and 10% (v/v) aqueous soap) using fresh human and male F344 rat skin in
flow-through diffusion cells.
All solutions were equally effective at removing MbOCA and MDA from the
surface of human skin,
with 21-47% of the applied dose removed at 72 hr. In contrast, with rat
skin 100% water and 1% soap
solution were significantly less (p < 0.05) effective than 10% soap
solution and 100% ethanol at
removing MbOCA and MDA. Washing the skin surface at 3 or 30 min
significantly reduced (p < 0.05)
the absorption of MbOCA and MDA into and through human and rat skin at 72
hr by two- to threefold,
compared with control unwashed skin. Washing the skin after this critical
time point did not significantly
reduce the absorption. These studies suggest that MbOCA and MDA are rapidly
absorbed from the skin
surface into the skin. Therefore, in order to reduce systemic exposure, the
skin must be washed within
the first 30 min after contamination has occurred. For human skin, the
choice of washing solution
employed was not as critical as the time of washing. This is in contrast to
the rat, where the higher
concentration soap and ethanol solutions were more effective for skin

PMID: 7657067, UI: 95385890

Contact Dermatitis 1995 May;32(5):303

Sensitivity to diaminodiphenylmethane.

Rudzki E, Rebandel P, Zawadzka A

Department of Dermatology, Warsaw School of Medicine, Poland.

PMID: 7634786, UI: 95361482

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