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EPA Preliminary Remedial Goals (PRG) 2003 Oct, air and tap water -- methanol, formaldehyde, formic acid -- sources omitted are methanol from aspartame, dark wines and liquors, fruit pectins: Murray 2005.01.18 rmforall
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| | From: | Rich Murray | | Subject: | EPA Preliminary Remedial Goals (PRG) 2003 Oct, air and tap water -- methanol, formaldehyde, formic acid -- sources omitted are methanol from aspartame, dark wines and liquors, fruit pectins: Murray 2005.01.18 rmforall | | Date: | 20 Jan 2005 18:10:27 -0000 |
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http://groups.yahoo.com/group/aspartameNM/message/1145
EPA Preliminary Remedial Goals (PRG) 2003 Oct, air and tap water --
methanol, formaldehyde, formic acid -- sources omitted are methanol from
aspartame, dark wines and liquors, fruit pectins: Murray 2005.01.18 rmforall
[ Introductory summary by Rich Murray: They gave the same data on
2004.10.27. I have put the data for methanol, formaldehyde, and formic acid
together in this plain text version, since oral ingestion of methanol,
whether from the 11% methanol component of aspartame, or the similar level
of methanol impurity in dark wines and liquors, about one part in ten
thousand, inevitably leads to full absorption in the human GI tract. Some
is excreted, but most is largely converted into formaldehyde, and thence
largely converted into formic acid -- both potent, culmulative toxins that
affect all cells and tissues.
Very large amounts of methanol are released by bacterial degradation of
pectins from fruits and vegetables in the human colon:
http://groups.yahoo.com/group/aspartameNM/message/1143
antiseptic? antifungal? antiviral? methanol (formaldehyde, formic acid)
disposition: Bouchard M et al, full plain text, 2001: substantial sources
are degradation of fruit pectins, liquors, aspartame, smoke: Murray
2005.01.05 rmforall
So, the key fact here is the RfDo, a lifetime safe level for daily ingested
oral exposure, which for these three chemicals are:
0.5 mg, 0.15 mg, and 2 mg per kg per day, which for a smallish adult of 60
kg, is 30 mg, 9 mg, and 120 mg daily for methanol, formaldehyde, formic
acid.
If about a third of any ingested oral methanol is turned into formaldehyde,
then the safety levels are comparable.
These safety limits suggest that ingested oral formic acid is about 12 times
less toxic than formaldehyde, but 4 times less toxic than methanol.
Yet, many reviews for decades say that methanol itself is not very toxic,
and that it is the resulting conversion into formaldehyde and thence into
formic acid, described as the major toxin, that results in a variety of
symptoms.
However, even if all the formaldedyde from methanol becomes formic acid, the
resulting toxicity would be about 4 times too low to account for the
putative methanol toxicity.
This kind of confusion and disharmony in various official safety limits for
these three chemicals, which are always largely transformed into each other
in the human body, is endemic in recent decades.
Official reviews all over the world make only indirect reference to the fact
that methanol is invariably a formaldehyde and formic acid source, and
almost never to the fact that dark wines and liquors and aspartame are
potent, ubiquitous sources for methanol, and even more so for the very large
amounts of methanol released by bacterial degradation of pectins from fruits
and vegetables in the human colon. Wood and tobacco smoke also contribute
substantial formaldehyde exposures.
I submit that this is because it is imperative for huge vested corporate
interests to keep confused, ignored, and unexplored the actual biochemical
disposition in specific tissues in vulnerable human groups of long-term,
chronic methanol, formaldehyde, and formic acid exposure from drinks, such
as dark wines and liquors, and aspartame diet drinks and many other
aspartame products.
In six years of reviewing this reseach, I have not found a single
published -- and here I emphasize the word "published" -- study of any
person or group that measures this.
This is outrageous.
Formaldehyde is a potent, cumulative toxin, neurotoxin, genotoxin,
officially declared human carcinogen, allergen, and hyper-sensitization
agent. It is addictive.
Aspartame is made of phenylalanine (50% by weight) and aspartic acid (39%),
both ordinary amino acids, bound loosely together by methanol (wood alcohol,
11%). Similar amounts of methanol in many fruits and vegetables, locked up
in complex pectin molecules, and always paired with ethanol, its natural
antidote, are not usually released by human digestion and so are harmless.
But the readily released methanol from aspartame is within hours largely
turned by the liver into formaldehyde and then formic acid, both potent,
cumulative toxins.
Fully 11% of aspartame is methanol -- 1,120 mg aspartame in 2 L diet soda,
almost six 12-oz cans, gives 123 mg methanol (wood alcohol). However,
about 30% of the methanol remains in the body as cumulative durable toxic
metabolites of formaldehyde and formic acid, 37 mg daily, a gram every
month, accumulating in and affecting every tissue.
If only 10% of the methanol accumulates daily as formaldehyde, that would
give 12 mg daily formaldehyde accumulation-- about 60 times more than the
0.2 mg from 10% retention of the 2 mg EPA daily limit for formaldehyde in
drinking water.
Bear in mind that the EPA limit for formaldehyde in drinking water is
1 ppm, or 2 mg daily for a typical daily consumption of 2 L of water.
http://groups.yahoo.com/group/aspartameNM/message/835
ATSDR: EPA limit 1 ppm formaldehyde in drinking water July 1999:
Murray 2002.05.30 rmforall
This is the same limit published May 2, 2002 for California
http://www.atsdr.cdc.gov/tfacts111.html [excerpts]
Agency for Toxic Substances and Disease Registry
Division of Toxicology
1600 Clifton Road NE, Mailstop E-29
Atlanta, GA 30333 888-422-8737 FAX: (404)498-0057
ATSDRIC@cdc.gov
http://www.atsdr.cdc.gov/contacts.html
Dr. Christopher T. De Rosa, Director, Division of Toxicology
(404) 498-0160 Fax: (404) 498-0094 cyd0@cdc.gov
Spengler, Robert, Sc.D., Associate Administrator for Science
(404) 498-0003 FAX: (404) 498-0081 : RSpengler@cdc.gov
http://www.atsdr.cdc.gov/science/bscroster01.html
Board of Scientific Counselors Roster June 2001
http://www.atsdr.cdc.gov/COM/omweb.html
Mr. Ronnie D. Wilson, the ATSDR Ombudsman
(404) 498 0004 (888) 422 8737] Fax (404) 498 0083 RWilson2@cdc.gov
When all routine avenues have been
exhausted, the ATSDR ombudsman can be
called to impartially investigate, mediate,
and assist in areas where the "system" has
failed. In doing so, this office is not an
advocate for the interests of ATSDR, nor is
it an advocate for business, nor industry,
nor private citizens, nor any other
government entity. It is an advocate for
problem resolution.
ToxFAQsTM for Formaldehyde CAS# 50-00-0 July 1999
Has the federal government made recommendations to protect human health?
The EPA recommends that an adult should not drink water containing more
than 1 milligram of formaldehyde per liter of water (1 mg/L) for a
lifetime exposure, and a child should not drink water
containing more than 10 mg/L for 1 day or 5 mg/L for 10 days.
The Occupational Safety and Health Administration (OSHA) has set a
permissable exposure limit for formaldehyde of 0.75 parts per million
(ppm) for an 8-hour workday, 40-hour workweek. [in air]
The National Institute for Occupational Safety and Health (NIOSH)
recommends an exposure limit of 0.016 ppm. [in air]
Source of Information:
Agency for Toxic Substances and Disease Registry (ATSDR). 1999.
Toxicological profile for formaldehyde. Atlanta, GA: U.S. Department of
Health and Human Services, Public Health Service.
http://www.atsdr.cdc.gov/toxprofiles/tp111.html July 1999
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http://groups.yahoo.com/group/aspartameNM/message/1111
Toxicological Profile for Formaldehyde 3/4 plain text, 229 to 342 of 468
pages USA DHHS PHS ATSDR 1999 July: Murray 2004.09.03 rmforall
This is really buried in the 1999 468-page ATSDR report:
" b. Water:
EPA 1-d Health Advisory (child)-draft 10 mg/L EPA 1995;
IRIS 1999 10-d Health Advisory (child)-draft 5 mg/L
Lifetime Health Advisory (adult)-draft 1 mg/L "
Four state water limits are 10 to 100 times more stringent:
" b. Water
Water Quality Criteria: Human Health
CA Drinking water (guideline) 30 µg/L FSTRAC 1995
MD Drinking water (guideline) 10 µg/L
ME Drinking water (guideline) 30 µg/L
NJ Drinking water (guideline) 100 µg/L "
FORMALDEHYDE page 338 7. REGULATIONS AND ADVISORIES
Table 7-1. Regulations and Guidelines Applicable to Formaldehyde (continued)
Agency Description Information References
Nonwastewater CMBST Guidelines:
a. Air:
ACGIH Ceiling Limit for Occupation Exposure
(TLV-STEL) 0.3 ppm (0.37 mg/m3) ACGIH 1998
NIOSH Recommended Exposure Limit for
Occupation Exposure (8-hr TWA) 0.016 ppm NIOSH 1992
Recommended Exposure Limit for
Occupation Exposure (15-min Ceiling) 0.1 ppm
Immediately Dangerous to Life and Health 20 ppm
b. Water:
EPA 1-d Health Advisory (child)-draft 10 mg/L EPA 1995; IRIS 1999
10-d Health Advisory (child) -- draft 5 mg/L
Lifetime Health Advisory (adult) -- draft 1 mg/L
Longer-term Health Advisory-draft 5 mg/L (child) 20 mg/L (adult)
d. Other:
ACGIH Group (Cancer Ranking) A2b ACGIH 1998
EPA Cancer Classification B1c IRIS 1999 RfD 0.2 mg/kg/day
NIOSH Cancer Classification Cad NIOSH 1992, 1994c
STATE
Regulations and Guidelines:
a. Air: Average Acceptable Ambient Air Concentrations EPA 1992c
AZ 1 hour 2x101 µg/m3
24 hours 1.2x101 µg/m3
FORMALDEHYDE page 339 7. REGULATIONS AND ADVISORIES
Table 7-1. Regulations and Guidelines Applicable to Formaldehyde (continued)
Agency Description Information References
STATE (cont.)
Annual 8x10-2 µg/m3
CT 8 hours 1.2x101 µg/m3
FL-FtLdle 8 hours 1.5x10-2 µg/m3
FL-Pinella 8 hours 4.5 µg/m3
24 hours 1.8 µg/m3
Annual 7.7x10-2 µg/m3
IN 8 hours 6 µg/m3
Annual 7.7x10-2 µg/m3
IN-Innap 8 hours 1.8x101 µg/m3
KS Annual 7.69x10-2 µg/m3
KS-KC Annual 7.69x10-2 µg/m3
LA Annual 7.69 µg/m3
MA 24 hours 3.3x10-1 µg/m3
Annual 8x10-2 µg/m3
ME 15 minutes 6.7x101 µg/m3
1 year 4x10-2 µg/m3
MI Annual 8x10-2 µg/m3
NC 15 minutes 1.5x10-1 µg/m3
NC-Forco 15 minutes 1.5x101 µg/m3
ND NA BACT
NV 8 hours 7.1x10-2 µg/m3
NY 1 year 5x10 µg/m3
OK 24 hours 1.2x101 µg/m3
PA-Phil 1 year 7.2 µg/m3
Annual 4.82 ppb
SC 24 hours 7.5 µg/m3
SD 8 hours 1.2x101 µg/m3
TX 30 minutes 1.5x101 µg/m3
Annual 1.5 µg/m3
VA 24 hours 1.2x101 µg/m3
VT Annual 8x10-2 µg/m3
WA-Olympia 5x10-2 ppm
STATE (cont.)
FORMALDEHYDE page 340 7. REGULATIONS AND ADVISORIES
Table 7-1. Regulations and Guidelines Applicable to Formaldehyde (continued)
Agency Description Information References
WA-SWEST Annual 7.7x10-2 µg/m3
b. Water
Water Quality Criteria: Human Health
CA Drinking water (guideline) 30 µg/L FSTRAC 1995
MD Drinking water (guideline) 10 µg/L
ME Drinking water (guideline) 30 µg/L
NJ Drinking water (guideline) 100 µg/L
a 2A = probable human carcinogen c B1 = probable human carcinogen
b A2 = suspected human carcinogen d Ca = potential occupational carcinogen
BACT = Best Available Control Technology;
BIF = Boilers and Industrial Furnaces; CARBN = Carbon adsorption;
CERCLA = Comprehensive Environmental Response, Compensation, and Liability
Act;
CHOXD = Chemical or electrolytic oxidation; CMBST = Combustion;
CWA = Clean Water Act; EPA = Environmental Protection Agency;
FDA = Food and Drug Administration;
FSTRAC = Federal State Toxicology and Regulatory Alliance committee;
FSUBS = Fuel Substitution; HAP = Hazardous Air Pollutants;
IARC = International Agency for Research on Cancer; INCIN = Incineration;
MCLG = Maximum Contaminant Level Goal; NA = not applicable;
NAS = National Academy of Sciences;
NESHAP= National Emission Standards for Hazardous Air Pollutants;
NIOSH = National Institute of Occupational Safety and Health;
NPDES = National Pollution Discharge Elimination System;
OAR - Office of Air and Radiation; ODW = Office of Drinking Water;
OERR = Office of Emergency and Remedial Response;
OSHA = Occupational Safety and Health Administration;
OSW = Office of Solid Wastes; OTS = Office of Toxic Substances;
PEL = Permissible Exposure Limit;
RCRA = Resource Conservation and Recovery Act;
RfD = Reference Dose; RQ = Reportable Quantities;
SOCMI = Synthetic Organic Chemicals Manufacturing Industry;
STEL = Short term exposure Limit; TLV= Threshold Limit Value;
TWA = Time-weighted Average; VOC = Volatile Organic Compound;
WHO = World Health Organization; WETOX = Wet Air Oxidation
No acute-duration oral MRL value was derived for formaldehyde.
A more detailed discussion of MRLs for formaldehyde is presented in Section
2.5 and in Appendix A of this profile.
The EPA oral reference dose (RfD) for formaldehyde is 0.2 mg/kg/day for
causing gastrointestinal damage.
No reference concentration (RfC) was reported for the compound (IRIS
1999).
The National Toxicology Program (1998) noted that formaldehyde is reasonably
anticipated to be a human carcinogen.
The International Agency for Research on Cancer (IARC) has classified
formaldehyde as 2A, probably carcinogenic to humans, based on limited
evidence of carcinogenicity in humans and sufficient evidence of
carcinogenicity in animals (IARC 1995).
The EPA has classified formaldehyde as a B1 compound, probable human
carcinogen based on limited evidence in humans and sufficient evidence in
animals (EPA 1991a; IRIS 1999).
FORMALDEHYDE page 341 7. REGULATIONS AND ADVISORIES
Formaldehyde is on the list of chemicals subject to the requirements of "The
Emergency Planning and Community Right-to-Know act of 1986" (EPCRA) (EPA
1988a).
Section 313 of Title III of EPCRA,
requires owners and operators of certain facilities that manufacture,
import, process, or otherwise use the
chemicals on this list to report annually their release of those chemicals
to any environmental media (U.S. Congress 1986).
OSHA requires employers of workers who are occupationally exposed to
formaldehyde to institute engineering controls and work practices to reduce
and maintain employee exposure at or below permissible exposure limits
(PELs).
The employer must use controls and practices, if feasible, to reduce
exposure to or below an 8-hour time-weighted average (TWA) of 0.75 ppm.
The 15-minute, short-term exposure limit (STEL) for formaldehyde is 2 ppm
(OSHA 1992).
The EPA regulates formaldehyde under the Clean Air Act (CAA) and has
designated formaldehyde as a hazardous air pollutant (HAP).
The major source category for which formaldehyde emissions are
controlled is the synthetic organic chemicals manufacturing industry
(SOCMI) -- equipment leaks, air oxidation unit processes, and distillation
operations (EPA 1983a, 1990a, 1990b).
Formaldehyde is regulated by the Clean Water Effluent Guidelines as stated
in Title 40, Section 414, of the Code of Federal Regulations (EPA 1987a).
The point source category for which specific Regulatory Limitations are
listed is the waste water discharge from the manufacture of formaldehyde as
a commodity organic chemical (EPA 1987a).
The Resource Conservation and Recovery Act (RCRA) identifies formaldehyde as
a toxic waste if it is discarded as a commercial product, manufacturing
intermediate, or off-specification commercial chemical product. Formaldehyde
is assigned the hazardous waste number, U122 (EPA 1980).
Under the Comprehensive Environmental Response, Compensation, and Liability
Act (CERCLA), owners of vessels or facilities are required to immediately
report release of formaldehyde equal to or greater than the reportable
quantity of 100 pounds (45.4 kg) (EPA 1985a).
When formaldehyde is used as a post-harvest fungicide for various raw
agricultural commodities that are used only as animal feed (e.g.,
barley, corn, rye grass soybean hay, and oats), the Federal Insecticide,
Fungicide, and Rodenticide Act (FIFRA) exempts formaldehyde from the
tolerance requirement for residues in or on the commodity (EPA 1975).
FORMALDEHYDE page 342 7. REGULATIONS AND ADVISORIES
The Food and Drug Administration (FDA) identifies formaldehyde as an
indirect food additive for use only as a component of adhesives (FDA 1977a).
When used in accordance with specified conditions, the food additive
formaldehyde may be safely used in the manufacture of animal feeds (FDA
1976). [ Continued ]
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http://groups.yahoo.com/group/aspartameNM/message/1108
faults in 1999 July EPA 468-page formaldehyde profile:
Elzbieta Skrzydlewska PhD, Assc. Prof., Medical U. of Bialystok, Poland,
abstracts -- ethanol, methanol, formaldehyde, formic acid, acetaldehyde,
lipid peroxidation, green tea, aging, Lyme disease:
Murray 2004.08.08 rmforall
Rich Murray, MA Room For All rmforall@comcast.net
1943 Otowi Road, Santa Fe, New Mexico 87505 USA 505-501-2298
Herein I offer abstracts and three full texts of dozens of studies by a
world-class biochemist and her associates, mostly experiments with rats, on
ethanol toxicity since 1984 and methanol toxicity since 1993. Enough
details are provided to show the competency and credibility of E.
Skrzydlewska and her colleagues over two decades, and to make access to
their literature more convenient for professionals.
For instance, anyone can click on this post at the above URL, and in Outlook
Express, use Control F to search the text for any word. Yahoo Groups also
includes a fine search function.
A conscientious, responsible review of any reseach that affects the
interests of vast commercial vested interests has to provide justified
criticism of dubious studies, reviews, and conclusions, that are
characteristically the main sources for private and professional
information. My experience since I first started investigating toxicity
issues in 1999 is, count on it, wolves guard the sheep.
To be effective, this criticism has to be calm, civil, detailed, specific,
reasonable, founded on evidence, focused on issues and not on persons, and
based on easily accessed public sources, so that anyone interested in basing
their conclusions on facts can start the laborous process of deciding for
themselves.
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Red wine contains twice as much methanol as does diet soda as an impurity,
about one part in ten thousand. It is the natural conversion by the body of
this methanol into formaldehyde and formic acid that is the main cause of
the well known "morning after" hangover symptoms: headache, nausea,
weakness, impaired memory, irritability, anxiety, "brain fog", body pains --
the same symptoms as aspartame victims.
Jones AW.
Elimination half-life of methanol during hangover.
Pharmacol Toxicol. 1987 Mar; 60(3): 217-20. PMID: 3588516
" But higher blood-methanol concentrations are definitely associated with
higher blood-ethanol in this sample of Swedish drinking drivers.
Frequent exposure to methanol and its toxic products of metabolism,
formaldehyde and formic acid, might constitute an additional health risk
associated with heavy drinking in predisposed individuals. " Jones AW 1988
Forensic Sci Int. 1988 Jun; 37(4): 277-85.
Relationship between the concentration of ethanol and methanol in blood
samples from Swedish drinking drivers.
Jones AW, Lowinger H.
Department of Alcohol Toxicology, University Hospital, Linkoping, Sweden.
Jones AW has 341 items in PubMed.
http://groups.yahoo.com/group/aspartameNM/message/1106
hangover research relevant to toxicity of 11% methanol in aspartame
(formaldehyde, formic acid): Calder I (full text): Jones AW: also some
methanol from fruit pectin in colon: Murray 2004.09.11 rmforall
http://bmj.bmjjournals.com/search.dtl search to get free full text
British Medical Journal 1997 (4 January); 314(7073): 2.
Ian Calder, F.R.C.A. [ Tel/Fax: 0171 720 9279 Consultant Anaesthetist at
the National Hospital for Neurology and Neurosurgery,
London WCIN 3BG, UK ]
Editorials Hangovers: Not the ethanol - perhaps the methanol
" Pawan compared the hangover produced by different types of drink (but only
one brand of each) in his study of 20 volunteers. The severity of hangover
symptoms declined in the order of brandy, red wine, rum, whisky, white wine,
gin, vodka, and pure ethanol.(6) Vodka and pure ethanol caused only mild
headaches in two volunteers. "
6. Pawan GL.
Alcoholic drinks and hangover effects.
Proc Nutr Soc 1973 May; 32: 15A. PMID: 4760771
J.A. Oppermann's Searle Co. lab proved that 30% of the methanol in
aspartame fed once to monkeys remained -- surely as formaldehyde and formic
acid in all tissues (1973, 1976, 1979).
http://groups.yahoo.com/group/aspartameNM/message/1088 Murray, full plain
text & critique: chronic aspartame in rats affects memory, brain cholinergic
receptors, and brain chemistry, Christian B, McConnaughey M et al, 2004 May:
2004.06.05 Pharmacol Biochem Behav. 2004 May; 78(1): 121-7. PMID: 15159141
Mona M. McConnaughey, Ph.D. Research Assistant Professor 252-744-2756
mcconnaugheym@mail.ecu.edu
Twelve rats fed aspartame at otherwise nontoxic levels for 4 months forgot
how to turn right to get a treat, and had specific brain changes.
http://groups.yahoo.com/group/aspartameNM/message/1067 eyelid contact
dermatitis by formaldehyde from aspartame, Hill AM & Belsito DV, Nov 2003:
Murray 2004.03.30 Contact Dermatitis. 2003 Nov; 49(5): 258-9. PMID:
14996049 A mysterious dermatitis was caused by a dose the same as two
packets Equal daily.
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http://groups.yahoo.com/group/aspartameNM/message/1131
genotoxicity of aspartame in human lymphocytes 2004.07.29 full plain text,
Rencuzogullari E et al, Cukurova University, Adana, Turkey 2004 Aug: Murray
2004.11.06 rmforall
[ Comments and corrections by Rich Murray are in square brackets. Spacing
has been added, without changing text, to increase readability and clarity,
and add emphasis. ]
Obviously, it hardly is conclusive to simply place aspartame in contact with
isolated living cells, without doing detailed explorations to determine the
degree of disassociation into phenylalanine, aspartic acid, and methanol,
with resulting formation of formaldehyde and formic acid,
as well as studying long-term accumulations in animals and humans --
except as a very valuable initial pilot study.
Nevertheless, their evidence and conclusions are devastating.
Rich Murray, MA Room For All rmforall@comcast.net
1943 Otowi Road, Santa Fe, New Mexico 87505 USA 505-501-2298
http://groups.yahoo.com/group/aspartameNM/messages
139 members, 1,147 posts in a public searchable archive also Co-Moderator
http://groups.yahoo.com/group/aspartame/messages bryanth@brooksdata.net
Aspartame Victims Support Group Edward Bryant Holman,
Chief Moderator 816 members, 17,947 posts in a public, searchable archive
http://www.presidiotex.com/aspartame/ bryanth@presidiotex.net
http://www.HolisticMed.com/aspartame mgold@holisticmed.com
Aspartame Toxicity Information Center Mark D. Gold also Co-Moderator
12 East Side Drive #2-18 Concord, NH 03301 603-225-2110
http://www.holisticmed.com/aspartame/abuse/methanol.html
"Scientific Abuse in Aspartame Research"
http://groups.yahoo.com/group/aspartameNM/message/957
safety of aspartame Part 1/2 12.4.2: EC HCPD-G SCF:
Murray 2003.01.12 rmforall EU Scientific Committee on Food, a whitewash
http://groups.yahoo.com/group/aspartameNM/message/1045
http://www.holisticmed.com/aspartame/scf2002-response.htm
Mark Gold exhaustively critiques European Commission Scientific
Committee on Food re aspartame ( 2002.12.04 ): 59 pages, 230 references
***************************************************************
"Schwartz ( 1999 ) also reported that methanol is converted to formaldehyde
which then accumulates in the cells.
Formaldehyde has been considered an inducer of cancer and acts to alter DNA
( Ewertz, 1993; Ewertz and Gill, 1990 ).
Olney et al. ( 1996 ) reviewed and explained that ASP had mutagenic
potential.....
In this study, we found that, ASP did appear to have genotoxic potential
consistent with potential carcinogenicity.
According to these results, phenyalanine and methanol, which are metabolic
products of ASP, have a genotoxic risk for humans.
In contrast, ASP was not found as a mutagen in in vivo studies.
However, in the present study, ASP induced CA and micronuclei in human
lyphocytes dose-dependently.
ASP did not change the osmolality of the medium at the maximum
concentrations ( 346 milliosmol) when compared with untreated medium (342
milliosmol ).
It was reported that a deviation from physiological osmolality
( approximately 300 milliosmol ) can lead to genotoxic effects
( Nowak, 1984, 1997; Seeberg et al., 1989 ).
According to these results, we can conclude that ASP induced CA and
percentage of micronuclei by itself because it did not alter the pH and
osmolality of the medium.
As shown, there are several contradictory studies about genotoxicity and
carcinogenicity of ASP.
However, it must be taken into account that ASP induced the CA and
micronuclei formation in a dose-dependent manner.
It is not possible to conclude that ASP is safe according to these results.
Therefore, it is necessary to be careful when using it in food and beverages
as a sweetener."
Genotoxicity of aspartame 2004.07.29 plain text, Rencuzogullari E et al,
Cukurova University, Adana, Turkey 2004 Aug
Drug Chem Toxicol. 2004 Aug; 27(3): 257-68.
Genotoxicity of aspartame. reyyup@mail.cu.edu.tr
Rencuzogullari E, Tuylu BA, Topaktas M, Ila HB, Kayraldiz A, Arslan M, Diler
SB. Biology Department, Faculty of Arts and Sciences,
Natural and Applied Sciences Institute, Cukurova University, Adana, Turkey.
****************************************************************
ATSDR 1999 July formaldehyde in tissues citations
*Galli CL, Ragusa C, Resmini P, et al.
1983. Toxicological evaluation in rats and mice of the ingestion
of a cheese made from milk with added formaldehyde.
Food Chem Toxicol 21: 313-317.
*Buckley KE, Fisher LJ, MacKay VG.
1988. Levels of formaldehyde in milk, blood, and tissues of dairy
cows and calves consuming formalin-treated whey.
J Agric Food Chem 36: 1146-1150.
*Jeffcoat AR, Chasalow F, Feldman DB.
1983. Disposition of [14C] formaldehyde after topical exposure
to rats, guinea pigs, and monkeys.
In: Gibson JE, ed. Formaldehyde toxicity.
Washington, DC: Hemisphere Publishing Corporation, 38-50.
*Heck Hd'A, Casanova M.
1987. Isotope effects and their implications for the covalent binding of
inhaled [3H]- and [14C]formaldehyde in the rat nasal mucosa.
Toxicol Appl Pharmacol 89: 122-134.
*Heck Hd'A, Casanova M.
1994. Nasal dosimetry of formaldehyde: Modeling site specificity and the
effects of preexposure.
Inhal Toxicol 6: 159-175.
Heck Hd'A, Casanova-Schmitz M.
1983. Biochemical toxicology of formaldehyde.
In: Hodgson, Bend, Philpot, ed.
Reviews in biochemical toxicology. New York, NY: Elsevier, 155-189.
Heck Hd'A, Keller DA.
1988. Toxicology of formaldehyde. ISI Atlas Sci
Pharmacol 2: 5-9.
Heck Hd'A, Casanova M, McNulty MJ, et al.
1986. Mechanisms of nasal toxicity induced by formaldehyde and acrolein.
In: Barrow CS, ed. Toxicology of the nasal passages.
Washington, DC: Hemisphere Publishing Corporation, 235-247.
*Heck Hd'A, Casanova M, Starr TB.
1990. Formaldehyde toxicity - new understanding.
CRC Crit Rev Toxicol 20: 397-426.
*Heck Hd'A, Casanova M, Steinhagen WH et al.
1989. DNA-protein cross-linking studies in rats and nonhuman primates.
In: Feron VJ and Bosland MC, eds. Nasal carcinogenesis in rodents: Relevance
to human health risk. The Netherlands: Pudoc Wageningen, 159-164.
(Cited in EPA, 1991a)
*Heck Hd'A, Casanova-Schmitz M, Dodd PB, et al.
1985. Formaldehyde (CH2O) concentrations in the blood of humans and
Fischer-344 rats exposed to CH2O under controlled conditions.
Am Ind Hyg Assoc J 46: 1-3.
*Heck Hd'A, Chin TY, Schmitz MC.
1983. Distribution of [14C] formaldehyde in rats after inhalation exposure.
In: Gibson JE, ed. Formaldehyde toxicity.
Washington, DC: Hemisphere Publishing Corporation, 26-37.
*Heck Hd'A, White EL, Casanova-Schmitz M.
1982. Determination of formaldehyde in biological tissues by gas
chromatography/mass spectrometry. Biomed Mass Spectrom 9: 347-353.
*Barry JL, Tome D.
1991. Formaldehyde content of milk in goats fed
formaldehyde-treated soybean oatmeal. Food Addit Contam 8: 633-640.
*Casanova M, Heck Hd'A.
1987. Further studies of the metabolic incorporation
and covalent binding of inhaled [3H]- and [14C] formaldehyde in Fischer-344
rats: Effects of glutathione depletion. Toxicol Appl Pharmacol 89: 105-121.
Casanova M, Heck Hd'A.
1991. The impact of DNA-protein cross-linking studies on quantitative risk
assessments of formaldehyde. CIIT Act 11: 1-6.
Casanova M, Heck Hd'A.
1997. Lack of evidence for the involvement of formaldehyde in the
hepatocarcinogenicity of methyl tertiary-butyl ether in CD-1 mice.
Chem Biol Interact 105: 131-143.
Casanova M, Conolly RB, Heck Hd'A.
1996a. DNA-protein cross-links (DPC) and cell proliferation in B6C3F1 mice
but not Syrian golden hamsters exposed to dichloromethane:
Pharmacokinetics and risk assessment with DPX as dosimeter.
Fundam Appl Toxicol 31: 103-116.
*Casanova M, Deyo DF, Heck Hd'A.
1989. Covalent binding of inhaled formaldehyde to DNA in the nasal mucosa of
Fischer 344 rats: Analysis of formaldehyde and DNA by high-performance
liquid chromatography and provisional pharmacokinetic interpretation.
Fundam Appl Toxicol 12: 319-417.
*Casanova M, Deyo DF, Heck Hd'A.
1992. Dichloromethane (methylene chloride):
Metabolism to formaldehyde and formation of DNA-protein cross links in
B6C3F1 mice and Syrian golden hamsters.
Toxicol Appl Pharmacol 114: 162-165.
*Casanova M, Heck Hd'A, Everitt JI, et al.
1988. Formaldehyde concentrations in the blood of Rhesus monkeys after
inhalation exposure. Food Chem Toxicol 26: 715-716.
Casanova M, Heck Hd'A, Janszen D.
1996b. Comments on 'DNA-protein crosslinks, a biomarker of
exposure to formaldehyde-in vitro and in vivo studies' by Shaham et al.
[Letter]. Carcinogenesis 17: 2097- 2101.
*Casanova M, Morgan KT, Gross EA, et al.
1994. DNA-protein cross-links and cell replication at specific sites in the
nose of F344 rats exposed subchronically to formaldehyde.
Fundam Appl Toxicol 23: 525-536.
*Casanova M, Morgan KT, Steinhagen WH, et al.
1991. Covalent binding of inhaled formaldehyde to DNA in the respiratory
tract of Rhesus monkeys:
Pharmacokinetics, rat-to-monkey interspecies scaling,
and extrapolation to man. Fundam Appl Toxicol 17: 409-428.
Casanova-Schmitz M, Heck H.
1983. Effects of formaldehyde exposure on the extractability of DNA
from proteins in the rat nasal mucosa. Toxicol Appl Pharmacol 70: 121-132.
*Casanova-Schmitz M, Raymond MD, Heck H d'A.
1984b. Oxidation of formaldehyde and acetaldehyde by NAD+-dependent
dehydrogenases in rat nasal mucosal homogenates.
Biochem Pharmacol 33: 1137-1142.
*Casanova-Schmitz M, Starr TB, Heck Hd'A.
1984a. Differentiation between metabolic incorporation and covalent binding
in the labeling of macromolecules in the rat nasal mucosa and bone marrow by
inhaled [14C]- and [3H] formaldehyde. Toxicol Appl Pharmacol 76: 26-44.
Swenberg JA, Heck Hd'A, Morgan KT, et al.
1985. A scientific approach to formaldehyde risk assessment.
In: Hoel DG, Merrill RA, Perera FP, ed. Risk quantitation and regulatory
policy.
Cold Spring Harbor, New York: Cold Spring Harbor Laboratory, 255-267.
*Swenberg JA, Kerns WD, Mitchell RI, et al.
1980. Induction of squamous cell carcinomas of the rat nasal cavity by
inhalation exposure to formaldehyde vapor. Cancer Res 40: 3398-3402.
Monticello TM.
1991. Formaldehyde-induced pathology and cell proliferation [Abstract].
Diss Abstr Int B 52: 2509-B.
Monticello TM, Morgan KT.
1989. Cell kinetics and characterization of
'preneoplastic' lesions in nasal respiratory epithelium of rats exposed to
formaldehyde [Abstract]. Carcinogenesis 30: 195.
Monticello TM, Morgan KT.
1994. Cell proliferation and formaldehyde-induced respiratory
carcinogenesis. Risk Anal 14: 313-319.
Monticello TM, Morgan KT.
1997. Chemically-induced nasal carcinogenesis and epithelial cell
proliferation: a brief review. Mutat Res 380: 33-41.
Monticello TM, Gross EA, Morgan KT.
1993. Cell proliferation and nasal carcinogenesis.
Environ Health Perspect 101(Suppl. 5): 121-124.
*Monticello TM, Miller FJ, Morgan KT.
1991. Regional increases in rat nasal epithelial cell proliferation
following acute and subchronic inhalation of formaldehyde.
Toxicol Appl Pharmacol 111: 409-421.
*Monticello TM, Morgan KT, Everitt JI, et al.
1989. Effects of formaldehyde gas on the respiratory tract of Rhesus
monkeys. Am J Pathol 134: 515-527.
*Monticello TM, Swenberg JA, Gross EA, et al.
1996. Correlation of regional and nonlinear formaldehyde-induced nasal
cancer with proliferating populations of cells.
Cancer Res 56: 1012-1022.
*Johannsen FR, Levinskas GJ, Tegeris AS.
1986. Effects of formaldehyde in the rat and dog following oral exposure.
Toxicol Lett 30:1-6.
Thrasher JD, Broughton A, Gard Z.
1988a. Indoor formaldehyde and the elderly. Clin Gerontol 7: 63-66.
*Thrasher JD, Broughton A, Micevich P.
1988b. Antibodies and immune profiles of individuals occupationally exposed
to formaldehyde six case reports. Am J Ind Med 14: 479-488.
*Thrasher JD, Broughton A, Madison R.
1990. Immune activation and autoantibodies in humans with long-term
inhalation exposure to formaldehyde. Arch Environ Health 45: 217-223.
*Thrasher JD, Madison R, Broughton A, et al.
1989. Building-related illness and antibodies to albumin conjugates of
formaldehyde, toluene diisocyanate, and trimellitic anhydride.
Am J Ind Med 15: 187-196.
*Thrasher JD, Wojdani A, Cheung G, et al.
1987. Evidence for formaldehyde antibodies and altered cellular immunity in
subjects exposed to formaldehyde in mobile homes.
Arch Environ Health 42: 347-350.
Til HP, Woutersen RA, Feron VJ, et al.
1988a. Sub-acute (4-week) oral toxicity of acetaldehyde and formaldehyde in
rats [Abstract]. Hum Toxicol 7: 86.
*Til HP, Woutersen RA, Feron VJ, et al.
1988b. Evaluation of the oral toxicity of acetaldehyde and formaldehyde in a
4-week drinking-water study in rats. Food Chem Toxicol 26: 447-452.
*Til HP, Woutersen VJ, Feron V, et al.
1989. Two-year drinking-water study of formaldehyde in rats.
Food Chem Toxicol 27: 77-87.
*Tobe M, Natio K, Kurokawa Y.
1989. Chronic toxicity study on formaldehyde administered orally to rats.
Toxicology 56: 79-86.
****************************************************************
[ RfDo Reference dose oral (mg/kg-d) -- IRIS, HEAST, or NCEA
RfDi Reference dose inhaled (mg/kg-d) -- IRIS, HEAST, or NCEA ]
http://www.epa.gov/Region9/waste/sfund/prg/files/02table.pdf
04--Mar--2003 129K
[ see also http://www.epa.gov/Region9/waste/sfund/prg/files/02airwater.pdf
Ambient Air and Residential Tap Water
04-Mar-2003 50K [ same values, with more info ] and
04airwater.pdf 27-Oct-2004 190K [ same values this year ]
http://www.epa.gov/Region9/waste/sfund/prg/files/02userguide.pdf [ quotes
below ]
EPA Region 9 PRGs Table 8 10/01/02
Key: SFo, i = Cancer Slope Factor oral, inhalation
RfDo, i = Reference Dose oral, inhalation i=IRIS h=HEAST n=NCEA
x=Withdrawn o=Other EPA Source r=Route-extrapolation
ca=Cancer PRG nc=Noncancer PRG
ca* (where: nc < 100X ca) ca**(where: nc < 10X ca)
+++=Non-Standard Method Applied
(See Section 2.3 of the "Region 9 PRGs Table User's Guide")
sat=Soil Saturation (See Section 4.5) max=Ceiling limit (See Section 2.1)
DAF=Dilution Attenuation Factor (See Section 2.5)
CAS=Chemical Abstract Services
CONTAMINANT ___ CAS No.
Methanol __________ 67-56-1
Formaldehyde ______ 50-00-0
Formic Acid ________ 64-18-6
TOXICITY INFORMATION [ 0 = oral i = inhaled ]
SFo ______ : RfDo ____ : SFi : ____ : RfDi :
VOC
skin : abs. : soils :
1/(mg/kg-d) : (mg/kg-d) : 1/(mg/kg-d) : (mg/kg-d) :
______ _ : 5.0E-01 i : _____ _ : 5.0E-01 :
_________ 0.5 mg __________ 0.5 mg
r : 0 : 0.10 :
_______ _ : 1.5E-01 i : 4.6E-02 i : ______ :
_________ 0.15 mg __ 0.046 mg
_ : 0 : 0.10 :
_______ _ : 2.0E+00 h : ______ _ : 2.0E+00 :
_________ 2.0 mg ____________ 2.0 mg
r : 0 : 0.10 :
PRELIMINARY REMEDIAL GOALS (PRGs)
"Direct Contact Exposure Pathways"
[ ingested ]
Residential _____ Industrial ______ Ambient Air ____ Tap Water
Soil (mg/kg) ____ Soil (mg/kg) ____ (ug/m^3) _______ (ug/l)
3.1E+04 nc _____ 1.0E+05 max ____ 1.8E+03 nc ____ 1.8E+04 nc
3 gm __________ 100 gm ________ 1.8 mg ________ 18 mg
9.2E+03 nc _____ 1.0E+05 nc _____ 1.5E-01 ca _____ 5.5E+03 nc
9.2 gm ________ 100 gm _________ 0.15 mg _______ 5.5 mg
1.0E+05 max ____ 1.0E+05 max ___ 7.3E+03 nc _____ 7.3E+04 nc
100 gm ________ 100 gm _________ 7.3 mg _________ 73mg
[ This table assumes that an adult breathes in and largely retains any
volatile chemicals in 20 m^3 daily, and ingests any chemicals from 2 L
drinking water or equivalent drinks daily.
So, the above safety limits for Ambient Air and [ ingested ] Tap Water,
converted to daily use, regardless of adult body weight, agree for methanol
and formic acid, and for formaldehyde, using a more sensitive cancer limit,
are about half as high for air as for water, a noncancer limit:
[ ingested ] Tap Water 36 mg, 11 mg, 146 mg
-- close to the RfDo for a 60 kg person.
So, the key fact here is the RfDo, a lifetime safe level for daily ingested
oral exposure, which for these three chemicals are:
0.5 mg, 0.15 mg, and 2 mg per kg per day, which for a smallish adult of 60
kg, is 30 mg, 9 mg, and 120 mg daily for methanol, formaldehyde, formic
acid. ]
SOIL SCREENING LEVELS
"Migration to Ground Water"
DAF 20 DAF 1
(mg/kg) (mg/kg) [ no values for these three chemicals ]
***************************************************************
http://www.epa.gov/Region9/waste/sfund/prg/files/02userguide.pdf
03-Oct-2002 157K 29 pages
UNITED STATES ENVIRONMENTAL PROTECTION AGENCY
REGION IX 75 Hawthorne Street, San Francisco, CA 94105
October 1, 2002
Subject: Region 9 PRGs Table 2002 Update
From: Stanford J. Smucker, Ph.D. smucker.stan@epa.gov
Regional Toxicologist (SFD-8-B)
Technical Support Team
To: PRGs Table Users
With this cover letter, we announce the update to the Region 9 PRGs table
for 2002.
The PRGs table contains over 600 preliminary remediation goals (PRGs) for
contaminants in soil, air, and tap water.
Region 9 PRGs are risk-based concentrations that are intended to assist risk
assessors and others in initial screening-level evaluations of environmental
measurements.
As their name implies, Region 9 PRGs may also be viewed as preliminary
cleanup goals for an individual chemical, but in this context, they are best
viewed as dynamic and subject to change because they are generic and based
on direct contact exposures which may not address site-specific conditions
and/or indirect exposure pathways at sites
(See Exhibit 1-1 in "Region 9 PRGs Table Users Guide/Technical Background
Document").
Also for planning purposes, these human health based PRGs should always be
considered in conjunction with ARAR-based PRGs (e.g. MCLs),
ecological benchmarks, and "background" conditions before establishing a
final cleanup level for a particular site.
You can find the PRGs 2002 table, InterCalc tables, "Region 9 PRGs Table
Users Guide/Technical Background Document", and additional helpful
toxicological and risk assessment information at:
http://www.epa.gov/region09/waste/sfund/prg/ .
We view risk-based PRGs as "evergreen".
Ongoing changes to the PRGs reflect continuing improvements in our
scientific knowledge base and state-of-the-art approaches to risk
assessment.
In the new Supplemental Guidance for Developing Soil Screening Levels for
Superfund Sites (Supplemental SSL Guidance, EPA 2001a), two different soil
ingestion rates are assumed for nonconstruction workers:
100 mg/day is assumed for outdoor workers
whereas 50 mg/day is assumed for indoor workers.
The default value of 100 mg/day for outdoor workers is also recommended by
EPA's Technical Review Workgroup for Lead (TRW),
and it reflects increased exposures to soils for outdoor workers
relative to their indoor counterparts.
For more on this, please see Section 4.1 of the
"Region 9 PRGs Table Users Guide/Technical Background Document"
or refer to the Supplemental SSL Guidance available at the following
website:
http://www.epa.gov/superfund/resources/soil/index.htm
Finally it should be recognized by all that use the PRGs table that not all
PRG values in the table are "created equal".
For some chemicals, a robust data set exists upon which the toxicological
criteria are based whereas for others, there may be relatively few studies
that form the basis of the PRG calculation.
Also, PRGs for some chemicals are based on withdrawn toxicity values or
route-extrapolated values.
Withdrawn and route-extrapolated numbers are shown in the table because we
still need to deal with these contaminants during the long delays before
replacement numbers are ready.
Please consult with your toxicologist or agency risk assessor to best
address potential uncertainties associated with chemical-specific PRGs,
especially if the chemical is a risk driver at your site.
page 3
1.0 INTRODUCTION
Region 9 Preliminary Remediation Goals (PRGs) are risk-based tools for
evaluating and cleaning up contaminated sites. They are being used to
streamline and standardize all stages of the risk decision-making process.
The Region 9 PRG table combines current EPA toxicity values with "standard"
exposure factors to estimate contaminant concentrations in environmental
media (soil, air, and water) that the agency considers protective of humans
(including sensitive groups), over a lifetime.
Chemical concentrations above these levels would not automatically designate
a site as "dirty" or trigger a response action.
However, exceeding a PRG suggests that further evaluation of the potential
risks that may be posed by site contaminants is appropriate.
Further evaluation may include additional sampling,
consideration of ambient levels in the environment,
or a reassessment of the assumptions contained in these screening-level
estimates (e.g. appropriateness of route-to-route extrapolations,
appropriateness of using chronic toxicity values to evaluate childhood
exposures, appropriateness of generic exposure factors for a specific site
etc.).
The PRG concentrations presented in the table can be used to screen
pollutants in environmental media,
trigger further investigation,
and provide an initial cleanup goal if applicable.
When considering PRGs as cleanup goals, residential concentrations should
be used for maximum beneficial uses of a property.
Industrial concentrations are included in the table as an alternative
cleanup goal for soils.
In general, it recommended that industrial PRGs not be used for screening
sites unless they are used in conjunction with residential values.
Before applying PRGs as screening tools or initial goals, the user of the
table should consider whether the exposure pathways and exposure scenarios
at the site are fully accounted for in the PRG calculations.
Region 9 PRG concentrations are based on direct contact pathways for which
generally accepted methods, models, and assumptions have been developed
(i.e. ingestion, dermal contact, and inhalation) for specific land-use
conditions and do not consider impact to groundwater or ecological receptors
(see Developing a Conceptual Site Model below).
2.0 READING THE PRG TABLE
2.1 General Considerations
With the exceptions described below, PRGs are chemical concentrations that
correspond to fixed levels of risk (i.e. either a one-in-one million [10-6]
cancer risk or a noncarcinogenic hazard quotient of 1) in soil, air, and
water.
In most cases, where a substance causes both cancer and noncancer
(systemic) effects, the 10-6 cancer risk will result in a more stringent
criteria and consequently this value is presented in the printed copy of the
table.
PRG concentrations that equate to a 10-6 cancer risk are indicated by "ca".
PRG concentrations that equate to a hazard quotient of 1 for noncarcinogenic
concerns are indicated by "nc".
If the risk-based concentrations are to be used for site screening, it is
recommended that both cancer and noncancer-based PRGs be used.
Both carcinogenic and noncarcinogenic values may be obtained
at the Region 9 PRG homepage at:
http://www.epa.gov/region09/waste/sfund/prg/
page 6
2.2 Toxicity Values
Hierarchy of Toxicity Values
EPA toxicity values, known as noncarcinogenic reference doses (RfD) and
carcinogenic slope factors (SF) were obtained from IRIS, NCEA through
September 2002, and HEAST (1997).
The priority among sources of toxicological constants in order of preference
is as follows:
(1) IRIS (indicated by "i"),
(2) NCEA ("n"),
(3) HEAST ("h"),
(4) withdrawn from IRIS or HEAST and under review ("x")
or obtained from other EPA documents ("o").
This hierarchy is subject to change once the HEAST tables are updated.
Inhalation Conversion Factors
As of January 1991, IRIS and NCEA databases no longer present RfDs or SFs
for the inhalation route.
These criteria have been replaced with reference concentrations (RfC) for
noncarcinogenic effects and unit risk factors (URF) for carcinogenic
effects.
However, for purposes of estimating risk and calculating risk-based
concentrations, inhalation reference doses (RfDi) and inhalation slope
factors (SFi) are preferred.
This is not a problem for most chemicals because the inhalation toxicity
criteria are easily converted.
To calculate an RfDi from an RfC, the following equation and
assumptions may be used for most chemicals:
RfDi mg/(kg-day) = RfC (mg/m^3) X 20 m^3/day X 1/70kg
Likewise, to calculate an SFi from an inhalation URF, the following equation
and assumptions may be used:
SFi (kg-day)/mg = URF (m^3/mcg) X day/20m^3 X 70kg X 10^3 mcg/mg
4.6 Tap Water - Ingestion and Inhalation
Calculation of PRGs for ingestion and inhalation of contaminants in domestic
water is based on the methodology presented in RAGS HHEM, Part B
(US EPA 1991a).
Ingestion of drinking water is an appropriate pathway for all chemicals.
For the purposes of this guidance, however, inhalation of volatile chemicals
from water is considered routinely only for chemicals with a Henry's Law
constant of 1 x 10-5 atm-m3/mole or greater and with a molecular weight of
less than 200 g/mole.
For volatile chemicals, an upperbound volatilization constant (VFw) is used
that is based on all uses of household water (e.g showering, laundering, and
dish washing).
Certain assumptions were made.
For example, it is assumed that the volume of water used in a residence for
a family of four is 720 L/day, the volume of the dwelling is 150,000 L and
the air exchange rate is 0.25 air changes/hour (Andelman in RAGS Part B).
Furthermore, it is assumed that the average transfer efficiency weighted by
water use is 50 percent (i.e. half of the concentration of each chemical in
water will be transferred into air by all water uses).
Note: the range of transfer efficiencies extends from 30% for toilets to 90%
for dishwashers.
EXHIBIT 4-1
STANDARD DEFAULT FACTORS
Symbol Definition (units) Default Reference
CSFo Cancer slope factor oral (mg/kg-d)-1 -- IRIS, HEAST, or NCEA
CSFi Cancer slope factor inhaled (mg/kg-d)-1 -- IRIS, HEAST, or NCEA
RfDo Reference dose oral (mg/kg-d) -- IRIS, HEAST, or NCEA
RfDi Reference dose inhaled (mg/kg-d) -- IRIS, HEAST, or NCEA
TR Target cancer risk 10-6 --
THQ Target hazard quotient 1 --
BWa Body weight, adult (kg) 70 RAGS (Part A), EPA 1989 (EPA/540/1-89/002)
BWc Body weight, child (kg) 15 Exposure Factors, EPA 1991 (OSWER No.
9285.6-03)
ATc Averaging time - carcinogens (days) 25550 RAGS(Part A), EPA 1989
(EPA/540/1-89/002)
ATn Averaging time - noncarcinogens (days) ED*365
SAa Exposed surface area for soil/dust (cm2/day) Dermal Assessment, EPA 2000
(EPA/540/R-99/005)
- adult resident 5700
- adult worker 3300
SAc Exposed surface area, child in soil (cm2/day) 2800 Dermal Assessment,
EPA 2000 (EPA/540/R-99/005)
AFa Adherence factor, soils (mg/cm2) Dermal Assessment, EPA 2000
(EPA/540/R-99/005)
- adult resident 0.07
- adult worker 0.2
AFc Adherence factor, child (mg/cm2) 0.2 Dermal Assessment, EPA 2000
(EPA/540/R-99/005)
ABS Skin absorption defaults (unitless):
- semi-volatile organics 0.1 Dermal Assessment, EPA 2000 (EPA/540/R-99/005)
- volatile organics -- Dermal Assessment, EPA 2000 (EPA/540/R-99/005)
- inorganics -- Dermal Assessment, EPA 2000 (EPA/540/R-99/005)
IRAa Inhalation rate - adult (m3/day) 20 Exposure Factors, EPA 1991 (OSWER
No. 9285.6-03)
IRAc Inhalation rate - child (m3/day) 10 Exposure Factors, EPA 1997
(EPA/600/P-95/002Fa)
IRWa Drinking water ingestion - adult (L/day 2 RAGS(Part A), EPA 1989
(EPA/540/1-89/002)
IRWc Drinking water ingestion - child (L/day) 1 PEA, Cal-EPA (DTSC, 1994)
IRSa Soil ingestion - adult (mg/day) 100 Exposure Factors, EPA 1991 (OSWER
No. 9285.6-03)
IRSc Soil ingestion - child (mg/day), 200 Exposure Factors, EPA 1991 (OSWER
No. 9285.6-03)
IRSo Soil ingestion - occupational (mg/day) 100 Soil Screening Guidance (EPA
2001a)
EFr Exposure frequency - residential (d/y) 350 Exposure Factors, EPA 1991
(OSWER No. 9285.6-03)
EFo Exposure frequency - occupational (d/y) 250 Exposure Factors, EPA 1991
(OSWER No. 9285.6-03)
EDr Exposure duration - residential (years) 30a Exposure Factors, EPA 1991
(OSWER No. 9285.6-03)
EDc Exposure duration - child (years) 6 Exposure Factors, EPA 1991 (OSWER
No. 9285.6-03)
EDo Exposure duration - occupational (years) 25 Exposure Factors, EPA 1991
(OSWER No. 9285.6-03)
Age-adjusted factors for carcinogens:
IFSadj Ingestion factor, soils ([mg-yr]/[kg-d]) 114 RAGS(Part B), EPA 1991
(OSWER No. 9285.7-01B)
SFSadj Dermal factor, soils ([mg-yr]/[kg-d]) 361
By analogy to RAGS (Part B)
InhFadj Inhalation factor, air ([m3-yr]/[kg-d]) 11
By analogy to RAGS (Part B)
IFWadj Ingestion factor, water ([L-yr]/[kg-d]) 1.1
By analogy to RAGS (Part B)
VFw Volatilization factor for water (L/m3) 0.5 RAGS(Part B), EPA 1991 (OSWER
No. 9285.7-01B)
PEF Particulate emission factor (m3/kg) See below Soil Screening Guidance
(EPA 1996a,b)
VFs Volatilization factor for soil (m3/kg) See below Soil Screening Guidance
(EPA 1996a,b)
sat Soil saturation concentration (mg/kg) See below Soil Screening Guidance
(EPA 1996a,b)
____________
Footnote:
aExposure duration for lifetime residents is assumed to be 30 years total.
For carcinogens, exposures are combined for children (6 years) and
adults (24 years) .
page 28
REFERENCES
ASTM. 1995. Standard Guide for Risk-Based Corrective Action Applied at
Petroleum Release Sites. Designation E 1739 - 95. Philadelphia,
Pennsylvania.
Calabrese, E.J., H. Pastides, R. Barnes, et al. 1989. How much soil do young
children ingest: an epidemiologic study. In:
Petroleum Contaminated Soils, Vol. 2. E.J. Calabrese and P.T. Kostecki, eds.
pp. 363-417. Chelsea, MI, Lewis Publishers.
California EPA. 1994. Preliminary Endangerment Assessment Guidance Manual.
(PEA) Department of Toxic Substances Control, Sacramento, California.
California EPA. 1996. Guidance for Ecological Risk Assessment at Hazardous
Waste Sites and Permitted Facilities, Part A: Overview. Department of Toxic
Substances Control, Sacramento, California.
Cowherd, C., G. Muleski, P. Engelhart, and D. Gillette. 1985. Rapid
Assessment of Exposure to Particulate Emission from Surface Contamination.
EPA/600/8-85/002. Prepared for Office of Health and Environmental
Assessment, U.S. Environmental Protection Agency, Washington, DC. NTIS
PB85-1922197AS.
Davis, S., P. Waller, R. Buschom, J. Ballou, and P. White. 1990.
Quantitative estimates of soil ingestion in normal children between the ages
of 2 and 7 years: population-based estimates using Al, Si, and Ti as soil
tracer elements. Archives of Environmental Health 45:112-122.
Howard, P.H. 1990. Handbook of Environmental Fate and Exposure Data for
Organic Chemicals. Lewis Publishers, Chelsea Michigan.
U.S. EPA. 1988. Superfund Exposure Assessment Manual. EPA/540/1-88/001.
Office of Emergency and Remedial Response, Washington, DC.
U.S. EPA. 1990a. Subsurface Contamination Reference Guide. EPA/540/2-90/011.
Office of Emergency and Remedial Response, Washington, DC.
U.S. EPA 1990b. Exposure Factors Handbook. EPA/600/8089/043.
Office of Health and Environmental Assessment, Washington, DC.
U.S. EPA. 1991a. Risk Assessment Guidance for Superfund Volume 1: Human
Health Evaluation Manual (Part B,
Development of Risk-Based Preliminary Remediation Goals). Publication
9285.7-01B. Office of Emergency and Remedial Response, Washington, DC. NTIS
PB92-963333.
U.S. EPA. 1991b. Human Health Evaluation Manual, Supplemental Guidance:
Standard Default Exposure Factors.
Publication 9285.6-03. Office of Emergency and Remedial Response,
Washington, DC. NTIS PB91-921314.
U.S. EPA. 1992a Technical Support Document for Land Application of Sewage
Sludge; Volumes I and II. Office of Water,
Washington, DC. 822/R-93-001a,b.
U.S. EPA. 1992b Dermal Exposure Assessment: Principles and Applications.
EPA/600/8-91/011B. Office of Health and
Environmental Assessment, Washington, DC.
U.S. EPA 1994a. Estimating Exposure to Dioxin-Like Compounds. U.S. EPA
Office of Research and Development, EPA/600/6-88/005B.
U.S. EPA 1994b. Role of Ecological Assessment in the Baseline Risk
Assessment. OSWER Directive No. 9285.7-17.
Office of Solid Waste and Emergency Response, Washington, DC.
U.S. EPA. 1996a. Soil Screening Guidance: Technical Background Document.
EPA/540/R-95/128. Office of Emergency and Remedial Response, Washington, DC.
PB96-963502.
U.S. EPA. 1996b. Soil Screening Guidance: User's Guide. EPA/540/R-96/018.
Office of Emergency and Remedial Response, Washington, DC. PB96-963505.
U.S. EPA 1996c. Superfund Chemical Data Matrix. EPA/540/R-96/028. Office of
Solid Waste and Emergency Response, Washington, DC. PB94-963506.
U.S. EPA. 1997a. Health Effects Assessment Summary Tables (HEAST): Annual
Update, FY 1997. National Center For Environmental Assessment (NCEA), Office
of Research and Development and Office of Emergency and Remedial Response,
Washington, DC.
U.S. EPA. 1997b. Ecological Risk Assessment Guidance for Superfund: Process
for Designing and Conducting Ecological Risk Assessments, Interim Final.
EPA/540/R-97/006. Office of Solid Waste and Emergency Response, Washington,
DC. PB97-963211.
U.S. EPA. 2001a. Supplemental Guidance for Developing Soil Screening Levels
for Superfund Sites, Interim Guidance. OSWER 9355.4-24.
U.S. EPA. 2001b. Risk Assessment Guidance for Superfund Volume I: Human
Health Evaluation Manual (Part E, Supplemental Guidance for Dermal Risk
Assessment), Interim Guidance. EPA/540/R-99/005. Office of Solid Waste and
Emergency Response, Washington, DC. PB99-963312.
U.S. EPA. 2001c. Guidance for Characterizing Background Chemicals in Soil at
Superfund Sites (Draft) June 2001, EPA/540/R-01/003. Office of Solid Waste
and Emergency Response, Washington, DC.
U.S. EPA. 2002. Integrated Risk Information System (IRIS). Duluth, MN.
Van Wijnen, J.H., P. Clausing and B. Brunekreef. 1990. Estimated soil
ingestion by children. Environmental Research, 51:147-162.
****************************************************************
In the 468-page 1999 ATSDR formaldehyde review, there were many reports
about formaldehyde from tobacco and wood smoke, but none about alcohol
drinks, wine, liquor, hangover, aspartame, or bacterial degradation of
fruit pectins in the human colon:
http://groups.yahoo.com/group/aspartameNM/message/1112
Toxicological Profile for Formaldehyde 4/4 plain text, 343 to 468 of 468
pages USA DHHS PHS ATSDR 1999 July: References, Glossary, Appendices,
Figures, Tables: Murray 2004.09.04 rmforall
*Alexandersson R, Hedenstierna G. 1989. Pulmonary function in wood workers
exposed to formaldehyde: A prospective study.
Arch Environ Health 44: 5-11.
Godish T. 1989. Formaldehyde exposures from tobacco smoke: A review.
Am J Public Health 79:1044 - 1045.
Green DJ, Bascom R, Healey EM, et al. 1989. Acute pulmonary response in
healthy, nonsmoking adults to inhalation of formaldehyde and carbon.
J Toxicol Environ Health 28: 261 - 275.
*Green DJ, Sauder LR, Kulle TJ, et al. 1987. Acute response to 3.0 ppm
formaldehyde in exercising health nonsmokers and asthmatics.
Am Rev Respir Dis 135: 1261 - 1266.
*Kulle TJ. 1993. Acute odor and irritation response in health nonsmokers
with formaldehyde exposure. Inhal Toxicol 5: 323-332.
Kulle TJ, Green DJ, Sauder LR. 1986. Acute pulmonary effects of 3.0 ppm
formaldehyde in exercising healthy nonsmokers and asthmatics [Abstracts].
Am Rev Respir Dis 133: A 355.
*Kulle TJ, Sauder LR, Hebel JR, et al. 1987. Formaldehyde dose-response in
healthy nonsmokers. J Air Pollut Control Assoc 37: 919 - 924.
*Lofroth G, Burton RM, Forehand L, et al. 1989. Characterization of
environmental tobacco smoke. Environ Sci Technol 23: 610 - 614.
*Mansfield CT, Hodge BT, Hege RB, et al. 1977. Analysis of formaldehyde in
tobacco smoke by high performance liquid chromatography.
J Chromatogr Sci 15: 301 - 302.
Newsome JR, Norman V, Keith CH. 1965. Vapor phase analysis of tobacco
smoke. Tob Int: 102 - 110.
*NRC. 1986. National Research Council. Environmental tobacco smoke:
Measuring exposures and assessing health effects. Washington, DC: National
Academy Press.
Quackenboss JJ, Bronnimann D, Camilli AE, et al. 1988. Bronchial
responsiveness in children and adults in association with formaldehyde,
particulate matter, and environmental tobacco smoke exposures
[Abstract]. Am Rev Respir Dis 137: 253.
*Quackenboss JJ, Lebowitz MD, Michaud JP, et al. 1989. Formaldehyde exposure
and acute health effects study. Environ Int 15: 169 - 176.
*Radford T, Dalsis DE. 1982. Analysis of formaldehyde in shrimp by high
pressure-liquid chromatography. J Agric Food Chem 30: 600 - 602.
Rylander R. 1974. Pulmonary cell responses to inhaled cigarette smoke.
Arch Environ Health 29: 329 - 333
*Sauder LR, Chatham MD, Green DJ, et al. 1986. Acute pulmonary response to
formaldehyde exposure in healthy nonsmokers.
J Occup Med 28: 420 - 424.
Sauder LR, Green DJ, Chatham MD, et al. 1987. Acute pulmonary response of
asthmatics to 3.0 ppm formaldehyde. Toxicol Ind Health 3: 569 - 577.
*Sterling TD, Collett CW, Sterling EM. 1987. Environmental tobacco smoke and
indoor air quality in modern office work environments.
J Occup Med 29: 57 - 61.
*Triebig G, Zober MA. 1984. Indoor air pollution by smoke constituents - a
survey. Prev Med 13:570 - 581.
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http://groups.yahoo.com/group/aspartameNM/message/1143
antiseptic? antifungal? antiviral? methanol (formaldehyde, formic acid)
disposition: Bouchard M et al, full plain text, 2001: substantial sources
are degradation of fruit pectins, liquors, aspartame, smoke: Murray
2005.01.05 rmforall
"That substantial amounts of methanol metabolites or by-products are
retained for a long time is verified by Horton et al. (1992) who estimated
that 18 h following an iv injection of 100 mg/kg of 14C-methanol in male
Fischer-344 rats, only 57% of the dose was eliminated from the body.
>From the data of Dorman et al. (1994) and Medinsky et al. (1997), it can
further be calculated that 48 h following the start of a 2-h inhalation
exposure to 900 ppm of 14C-methanol vapors in female cynomolgus monkeys,
only 23% of the absorbed 14C-methanol was eliminated from the body.
These findings are corroborated by the data of Heck et al. (1983) showing
that 40% of a 14C-formaldehyde inhalation dose remained in the body 70 h
postexposure."
"Exposure to methanol also results from the consumption of certain
foodstuffs (fruits, fruit juices, certain vegetables, aspartame sweetener,
roasted coffee, honey) and alcoholic beverages (Health Effects Institute,
1987; Jacobsen et al., 1988)." [ It's unusual for a mainstream journal
article to mention"fruits, fruit juices, certain vegetables, aspartame
sweetener" and "alcoholic beverages" to be methanol sources.
Alcohol Clin Exp Res. 1997 Aug; 21(5): 939-43.
Endogenous production of methanol after the consumption of fruit.
Lindinger W, Taucher J, Jordan A, Hansel A, Vogel W.
Institut fur Ionenphysik, Leopold Franzens Universitat Innsbruck, Austria.
After the consumption of fruit, the concentration of methanol in the human
body increases by as much as an order of magnitude.
This is due to the degradation of natural pectin (which is esterified with
methyl alcohol) in the human colon.
In vivo tests performed by means of proton-transfer-reaction mass
spectrometry show that consumed pectin in either a pure form (10 to 15 g)
or a natural form (in 1 kg of apples) induces a significant increase of
methanol in the breath (and by inference in the blood) of humans.
The amount generated from pectin (0.4 to 1.4 g)
is approximately equivalent to the total daily endogenous production
(measured to be 0.3 to 0.6 g/day)
or that obtained from 0.3 liters of 80-proof brandy
(calculated to be 0.5 mg). [ 1667 mg methanol per liter of brandy ]
This dietary pectin may contribute to the development
of nonalcoholic cirrhosis of the liver. PMID: 9267548
Alcohol Clin Exp Res. 1995 Oct; 19(5): 1147-50.
Methanol in human breath.
Taucher J, Lagg A, Hansel A, Vogel W, Lindinger W.
Institut fur Ionenphysik, Universitat Innsbruck, Austria.
Using proton transfer reaction-mass spectrometry for trace gas analysis of
the human breath, the concentrations of methanol and ethanol have been
measured for various test persons consuming alcoholic beverages and various
amounts of fruits, respectively.
The methanol concentrations increased from a natural (physiological) level
of approximately 0.4 ppm up to approximately 2 ppm a few hours after eating
about 1/2 kg of fruits,
and about the same concentration was reached after drinking of 100 ml brandy
containing 24% volume of ethanol and 0.19% volume of methanol.
[ 24 ml = 64 mg ethanol and 0.19 ml = 0.33 g methanol = 340 mg methanol ]
PMID: 8561283 ]
"However, the severe toxic effects are usually associated with the
production and accumulation of formic acid, which causes metabolic acidosis
and visual impairment that can lead to blindness and death at blood
concentrations of methanol above 31 mmol/l (Røe, 1982; Tephly and McMartin,
1984; U.S. DHHS, 1993).
Although the acute toxic effects of methanol in humans are well documented,
little is known about the chronic effects of low exposure doses, which are
of interest in view of the potential use of methanol as an engine fuel and
current use as a solvent and chemical intermediate.
Gestational exposure studies in pregnant rodents (mice and rats) have also
shown that high methanol inhalation exposures (5000 or 10,000 ppm and more,
7 h/day during days 6 or 7 to 15 of gestation) can induce birth defects
(Bolon et al., 1993; IPCS, 1997; Nelson et al., 1985)."
[ There's an on-going debate as to how much of methanol toxicity and
genotoxicity is due to its formaldehyde or formic acid products, along with
a dearth of evidence about the actual biochemical disposition in specific
tissues of people exposed long-term to chronic doses, as in the case of
alcoholics or of aspartame reactors. ]
************************************************************
Rich Murray, MA Room For All rmforall@comcast.net
1943 Otowi Road, Santa Fe, New Mexico 87505 USA 505-501-2298
http://groups.yahoo.com/group/aspartameNM/messages
139 members, 1,147 posts in a public searchable archive also Co-Moderator
http://groups.yahoo.com/group/aspartame/messages bryanth@brooksdata.net
Aspartame Victims Support Group Edward Bryant Holman, Chief Moderator 816
members, 17,947 posts in a public, searchable archive
http://www.presidiotex.com/aspartame/ bryanth@presidiotex.net
http://www.HolisticMed.com/aspartame mgold@holisticmed.com
Aspartame Toxicity Information Center Mark D. Gold also Co-Moderator
12 East Side Drive #2-18 Concord, NH 03301 603-225-2110
http://www.holisticmed.com/aspartame/abuse/methanol.html
"Scientific Abuse in Aspartame Research"
http://groups.yahoo.com/group/aspartameNM/message/957
safety of aspartame Part 1/2 12.4.2: EC HCPD-G SCF:
Murray 2003.01.12 rmforall EU Scientific Committee on Food, a whitewash
http://groups.yahoo.com/group/aspartameNM/message/1045
http://www.holisticmed.com/aspartame/scf2002-response.htm
Mark Gold exhaustively critiques European Commission Scientific
Committee on Food re aspartame ( 2002.12.04 ): 59 pages, 230 references
http://groups.yahoo.com/group/aspartameNM/message/1133
Mark Gold, most recent of 14 Rapid Responses to Aspartame and its effects on
health, BMJ: Murray 2004.11.06 rmforall
http://groups.yahoo.com/group/aspartameNM/message/1124
8 more Rapid Responses to Aspartame and its effects on health, BMJ:
Murray 2004.10.18 rmforall
http://groups.yahoo.com/group/aspartameNM/message/1120
5 critical Rapid Responses to Aspartame and its effects on health, Michael E
J Lean and Catherine R Hankey, BMJ 2004; 329: 755-756:
Murray 2004.10.05 rmforall
http://groups.yahoo.com/group/aspartameNM/message/1117
Aspartame and its effects on health, Michael E.J. Lean, Catherine R. Hankey,
Glasgow UK, British Medical Journal: 11% methanol component of aspartame,
and same level of methanol in dark wines and liquors, turns to formaldehyde
and formic acid, the main cause of chronic hangover symptoms: Murray
2004.10.04 rmforall
http://bmj.bmjjournals.com/cgi/eletters/329/7469/755#76712
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