RE: MDI Emissions

["Jon Dettling" <dettling@glc.org>]

Anne,

That I'm aware of, our group has never addressed the use of MDI as a
spray-on truck liner, although there are certainly others on the group who
would have a longer and more detailed memory than me. The only exception
would be if these operations were large enough to require reporting of their
emissions.

Regarding toxicity, the following abstracts may be of some use. In
particular, the first of these states that MDI is a probable carcinogen and
was the only information I saw regarding carcinogenicity. It seems that it's
well established that it is a respiratory irritant at occupational exposure
levels, and apparently has also been linked to onset of asthma. The final
abstract below deals with its use in truck bed lining from an occupational
health perspective an may be of interest to you. It doesn't sound like it
would provide much insight into the ambient emissions from this process. I
didn't see much information about exposures in the ambient environment,
which is where I think it's listing as a HAP would be relevant. According to
the EPA's PBT profiler, it had moderate persistence and is moderately
bioacculuative in the environment, so multi-media risk considerations may be
an important consideration, especially if it is a carcinogen. The PBT
profiler gave not estimate of it's toxicity to aquatic life.

Jon

Bolognesi, C; Baur, X; Marczynski, B; Norppa, H; Sepai, O; Sabbioni, G.
2001. Carcinogenic risk of toluene diisocyanate and 4,4 '-methylenediphenyl
diisocyanate: Epidemiological and experimental evidence. CRITICAL REVIEWS IN
TOXICOLOGY 31 (6): 737-772.

Abstract: Diisocyanates are highly reactive compounds widely used, for
example, in the production of polyurethane foams, elastomers, paints, and
adhesives. The high chemical reactivity of these compounds is also reflected
in their toxicity: diisocyanates are one of the most important causes of
occupational asthma but also other adverse effects, such as irritation and
toxic reactions, have been described in exposed subjects. One of the open
questions is whether occupational isocyanate exposure is a carcinogenic
hazard. The few epidemiological studies available have been based on young
cohorts and short follow-up and are not conclusive. Toluene diisocyanate
(TDI) has been classified as carcinogenic in animals on the basis of gavage
administration studies, but no conclusions are available on inhalation
exposure. For 4,4'-methylene diphenyldiisocyanate (MDI) there is suggestive
evidence for carcinogenicity in rats. The possible carcinogenic mechanism of
TDI and MDI is not clear. Both chemicals have been positive in a number of
short-term tests inducing gene mutations and chromosomal damage. The
reactive form could be either the diisocyanate itself or may derive from the
metabolic activation of the aromatic diamine derivatives formed by
hydrolysis. TDI and MDI react with DNA in vivo and in vitro. However, the
structure of the adducts has not been identified. Especially from the in
vivo experiment it is not known if the adducts are a product from the
reaction with the isocyanate or the corresponding amine. In conclusion, both
TDI and MDI are highly reactive chemicals that bind to DNA and are probably
genotoxic. The alleged animal carcinogenicity of TDI and MDI would suggest
that occupational exposure to these compounds is a carcinogenic risk. The
few epidemiological studies available have not, however, been able to
clarify if TDI and MDI are occupational carcinogens.

Feron, VJ; Kittel, B; Kuper, CF; Ernst, H; Rittinghausen, S; Muhle, H; Koch,
W; Gamer, A; Mallett, AK; Hoffmann, HD. 2001. Chronic pulmonary effects of
respirable methylene diphenyl diisocyanate (MDI) aerosol in rats:
combination of findings from two bioassays. ARCHIVES OF TOXICOLOGY 75 (3):
159-175.

Abstract: Two independent bioassays are available which have examined the
potential carcinogenicity of monomeric and polymeric methylene diphenyl
diisocyanate (MDI) following long-term inhalation exposure in rats. These
studies are not directly comparable, however, due to differences in design
and conduct of the in-life phase, and differences in nomenclature used for
some of the histopathological findings. This paper presents a definitive
overview of the pulmonary toxicity of MDI developed following a thorough
review of both investigations. As part of this process, the test materials
and the designs of the studies were compared, and an in-depth review of lung
lesions was conducted by an independent reviewing pathologist. This included
the reexamination of the original lung slides, supported by an analysis of
the exposure regimens, the results of which were used to develop an accurate
profile of the doses received by the animals in the two studies.
Histopathological findings were then combined with this information to give
an overall dose-response curve for both studies as a whole. The range of
total inhalation exposures to MDI was calculated as 559, 1972, 2881, 6001,
17,575 and 17,728 mgh/m(3). Major pulmonary effects included increased lung
weights together with bronchiolo-alveolar adenomas and hyperplasia, and
interstitial fibrosis which occurred consistently in both studies,
indicating a very similar qualitative response of the lungs to polymeric and
monomeric MDI. The quantitative response of the lung was clearly
dose-related in each study, and when the studies were considered as a whole
a reasonable overall dose-response relationship was apparent for major lung
lesions. Lung tumours tin low incidences) only occurred at the highest dose
level in both studies (17,575 and 17,728 mgh/m(3)). For inflammatory and
other non-neoplastic pulmonary changes, the lowest dose examined (559
mgh/m(3)) was regarded as a no-observed-adverse-effect-level for both
polymeric and monomeric MDI. It was concluded that the results of the two
studies could be combined to serve as a basis for human risk assessment of
MDI.

Gamer, AO; Hellwig, J; Doe, JE; Tyl, RW. 2000. Prenatal toxicity of inhaled
polymeric methylenediphenyl diisocyanate (MDI) aerosols in pregnant Wistar
rats. TOXICOLOGICAL SCIENCES 54 (2): 431-440.

Abstract: Mated Wistar rats, 25/group, were exposed to polymeric
methylenediphenyl diisocyanate (MDI) aerosol of respirable size for 6 h/day,
on gestational days (gd) 6 through 15, at 0, 1, 4, and 12 mg/m(3). Maternal
clinical signs, body weights, and feed and water consumption were measured
throughout gestation. At scheduled sacrifice on gd 20, maternal body, gravid
uterine, liver, and paired lung weights were documented. Corpora lutea were
counted, implantation sites were identified: resorptions, dead and live
fetuses, and placentas were weighed. All live fetuses were counted, sexed,
weighed, and examined for external alterations; approximately 50% of the
live fetuses/litter were preserved in Bouin's fixative and examined for
visceral alterations, and the remaining live fetuses! litter were cleared
and stained with alizarin red S and examined for ossified skeletal
alterations. Maternal toxicity was observed at 12 mg/m(3), including
mortality (2 of 24 pregnant), damage to the respiratory tract, reduced body
weights and weight gain, reduced liver and increased lung weights, and
reduced gravid uterine weight (the last not statistically significantly
different from the control value). Developmental toxicity was also observed
at 12 mg/m(3), including reduced placental and fetal body weights and an
increased incidence of fetal skeletal variations and skeletal retardations.
There was no evidence of maternal or developmental toxicity at 1 or 4
mg/m(3). The no observed adverse effect concentration for maternal and
developmental toxicity was therefore 4 mg/m(3). There were no
treatment-related teratogenic effects at any concentrations evaluated.

Pauluhn, J; Emura, M; Mohr, U; Popp, A; Rosenbruch, M. 1999. Two-week
inhalation toxicity of polymeric diphenylmethane-4,4 '-diisocyanate (PMDI)
in rats: Analysis of biochemical and morphological markers of early
pulmonary response. INHALATION TOXICOLOGY 11 (12): 1143-1163.

Abstract: The pulmonary response of Wistar rats to respirable polymeric
diphenylmethane-4,4'-diisocyanate (PMDI) aerosol was examined in a 2-wk
repeated nose-only inhalation exposure study. Exposure concentrations were
1.1, 3.3, and 13.7 mg PMDI/m(3) (6 h/day, 15 exposures). The level of 13.7
mg/m(3) was actually a combination of an initial target concentration of 10
mg/m(3) in wk 1, which was raised to 16 mg/m(3) in wk 2, due to a lack of
signs suggestive of pulmonary irritation. An acute sensory irritation study
on rats served as basis for selection of these concentrations. Shortly after
the 2-wk expo sure period, rats were subjected to pulmonary function and
arterial blood gas measurements. Lungs were examined by light and
transmission electron microscopy, and labeling indices in terminal
bronchioles were measured. Bronchoalveolar lavage (BAL) was performed to
assess various indicators of pulmonary inflammation, including neutrophil
and macrophage numbers, protein, lactate dehydrogenase (LDH),
gamma-glutamyltranspeptidase (gamma-GT), alkaline phosphatase (APh), acid
phosphatase (ACPh), and beta-N-acetylglucosaminidase (beta-NAG).
Phosphatidylcholine in BAL fluid and BAL cells was determined as aggregated
endpoint suggestive of changes in pulmonary surfactant. Rats exposed to 3.3
and 13.7 mg/m(3) experienced concentration-dependent signs of respiratory
tract irritation. Determination of arterial blood gases, lung mechanics, and
carbon monoxide diffusing capacity did not demonstrate specific effects.
Analysis of BAL fluid and BAL cells revealed changes indicative of marked
inflammatory response and/or cytotoxicity in rats exposed to 13.7 mg/m(3),
and the changes were characterized by statistically significantly increased
activities of LDH, beta-NAG, and protein. Phospholipid concentrations were
increased in rats exposed to 1.1 mg/m(3) and above (elevated levels of lipid
material in alveolar macrophages demonstrated by polychrome stain) and 3.3
mg/m(3) and above (increased intracellular ACPh activity and intracellular
phospholipids). In these groups, gamma-GT was statistically significantly
increased. These findings suggest that changes in phospholipid homeostasis
appear to occur at lower levels than those eliciting inflammation and
cytotoxicity. Light and transmission electron microscopy suggest that
exposure to 3.3 and 13.7 mg/m(3) resulted in focal inflammatory lesions and
an accumulation of refractile, yellowish-brownish material in alveolar
macrophages with concomitant activation of type II pneumocytes. In the
terminal bronchioles a concentration-dependent increase of bromodeoxyuridine
(BrdU)-labeled epithelial cells was observed in ail PMDI exposure groups. in
summary, it appears that respirable PMDI aerosol interacts with pulmonary
surfactant, which, in turn, may stimulate type Ii pneumocytes to increase
their production of surfactant and to proliferate.


Lofgren DJ, Walley TL, Peters PM, and Weis ML. Appl Occup Environ Hyg. 2003
Oct;18(10):772-9.  MDI Exposure for Spray-On Truck Bed Lining.

Abstract:  Worker exposure to MDI (methylenediphenyl isocyanate) in the
sprayed-on truck bed lining industry was assessed by examining Washington
State OSHA inspection files and industrial insurance records. The industry
uses MDI to form a protective urethane coating on pick-up truck beds. The
lining is applied by a worker using a handheld spray gun with application
equipment at temperatures and pressures specified by the urethane supplier.
Inspections with MDI sampling were initially identified by searching the
agency's laboratory database and were further screened for the targeted
process. Data for 13 employers was found and extracted from the inspection
records. All were small companies with only 1 to 2 workers exposed to MDI;
10 of the 13 employers had started the bed lining service within the last 4
years. The process was found in truck bed lining specialty shops as well as
in other truck-related businesses. Six different urethane products were used
with reported MDI monomer concentrations of up to 75 percent along with
varying concentrations of MDI pre-polymers and other reactants and solvents.
Sampling for MDI by inspectors found 7 worksites with worker exposure in
excess of the state and OSHA ceiling limit of 0.200 mg/M(3). Deficiencies in
respirator programs and engineering controls for MDI were cited. A review of
the industrial insurance records found a total of five MDI-related claims at
4 inspected worksites, two for new-onset asthma. It was concluded that
workers in the urethane sprayed-on truck bed lining industry are at an
increased risk of developing illnesses associated with isocyanate exposure.
Interventions are needed to further assess the hazard as well as motivate
and assist franchisers, distributors, and retailers to implement effective
engineering controls and respiratory protection programs in this nationally
emerging small employer industry.
______________________
Jon Dettling
Great Lakes Commission
734-971-9135
dettling@glc.org

-----Original Message-----
From: Pope.Anne@epamail.epa.gov [mailto:Pope.Anne@epamail.epa.gov] 
Sent: Friday, October 27, 2006 7:29 AM
To: Wu, Chun Yi
Cc: Airtoxics; Wu, Chun Yi; dettling@glc.org;
owner-airtoxics@great-lakes.net
Subject: RE: MDI Emissions

Chun,

Can you send me your MDI revisions so that I can revise the 2002 NEI?
We have a delisting petition for MDI and I had highlighted MN data as a
discrepancy with petitioner's data .

Has the GLC looked at spray on truck bed liners as a source of MDI in
their inventory?  This is a new use of MDI and has not appeared in any
inventories yet.  We think it may a significant source of emissions as a
lot of small shops do this kind of activity.  CDC is concerned about
this new source of MDI as part of the petition, but we have no inventory
data.

There is also concern about sensitivity of individuals to MDI.  Studies
from CDC/OSHA show increased sensitivity to individuals who live near
facilities releasing MDI and to workers who use MDI.

I would interested in receiving any info you may have re health studies
on MDI or inventory data for spray on truck bed liners.

I hope your are doing well.  I wish our cold blast this week would go
back up to your area -- so our temps would return to the high
sixties/low seventies as they usually are.

Are you coming to the STAPPA/ALAPCO Air Toxics Workshop in December of
this year?  GLC may be interested in hearing about Residual Risk
Technology Rule and use of NEI data for individual facility risk
assessments that we have conducted.  I will be giving presentation and
demo at the workshop of review data base that will be published in FR in
late November/early December of this year.  Several of the categories
included in the rule have facilities in the GLC area.

anne


                                                                        
           
                                                                        
                                                                        
                                                                        
                                                                        
                                                                        
                                                                        





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