De: Raise in arsenic limit angers groups - Department increased allowable levels without formally notifying citizens

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{several citations follow the news item.}

Raise in arsenic limit angers groups

Department increased allowable levels without formally notifying citizens

By JEFF MONTGOMERY / The News Journal

02/22/2005

http://www.delawareonline.com/newsjournal/local/2005/02/22raiseinarsenicl.html

Citizen and environmental groups on Monday criticized a little-noticed

state action that raised the level of what is considered acceptable

arsenic pollution in Delaware soil, and said regulators should seek

public comment before changing standards.

The Department of Natural Resources and Environmental Control late last

year set a standard of 23 parts per million before it requires an

investigation into arsenic contamination or cleanup on commercial and

industrial property - up from an 11 ppm level adopted in 2002.

Common Cause of Delaware, the Civic League for New Castle County, the

Milltown-Limestone Civic Alliance and Green Delaware said in a news

conference in Wilmington that DNREC bypassed regulatory review

requirements with the decision, unilaterally increasing allowable levels

of exposure to a known cancer-causing element.

" I don't know how you can justify it, " said Flaherty, a lobbyist

for Common Cause of Delaware. " The overriding theme is, DNREC is

ignoring the public process. "

DNREC Deputy Secretary Small said the agency sets and adjusts soil

cleanup standards internally, rather than through formal public notice

and review actions. Acceptable arsenic levels have increased over the

years, Small said, as sampling and research have raised the level

considered to be natural or caused by industrial activities dating back

a century or more.

In some cases, arsenic levels in Delaware soil can be linked to

industrial activities dating to the 1800s. Wilmington-based tanneries

and foundries that served the 19th century railroad industry helped to

drive up arsenic levels in some areas. Large portions of the city stand

on former wetlands filled with arsenic-rich slag.

" One of the challenges in Delaware is that we have naturally occurring

arsenic levels that often are in the 11 ppm range, " Small said.

Wide differences among states have complicated the debate. Pennsylvania

currently allows up to 53 ppm for commercial and industrial property,

Michigan up to 48 ppm, Texas 200 ppm.

DNREC has conducted extensive arsenic contamination investigations in

recent years as redevelopment projects include properties that once were

tanneries or other industrial sites.

In neighborhoods near a golf course property off Hercules Road, now

under study for development, soil testing has raised concerns about

residual levels of pesticides, arsenic and other contaminants.

In a letter on the Hercules Road issue sent last year to Sen.

M. Blevins, D-Elsmere, and Rep. Deborah Hudson, R-Fairthorne, DNREC

Secretary A. said that a 4 ppm standard in place before 2002

was based on levels that might cause one additional cancer death after a

lifetime of exposure per 100,000 residents. The decision to increase the

standard to 11 ppm, wrote, was prompted by a concern that " we

wouldn't want responsible parties to have to clean up to levels that are

more conservative than what exists in the natural environment. "

Contact Jeff Montgomery at 678-4277 or jmontgomery@...

<mailto:jmontgomery@...>

*

0: Neuro Endocrinol Lett. 2002 Aug;23(4):303-8.

Treatment of autism spectrum children with thiamine tetrahydrofurfuryl

disulfide: a pilot study.

Lonsdale D, Shamberger RJ, Audhya T.

Preventive Medicine Group, 24700 Center Ridge Road, Westlake, OH 44145, USA.

dlonsdale@...

OBJECTIVES: In a Pilot Study, the clinical and biochemical effects of thiamine

tetrahydrofurfuryl disulfide (TTFD) on autistic spectrum children were

investigated. SUBJECTS AND METHODS: Ten children were studied. Diagnosis was

confirmed through the use of form E2, a computer assessed symptom score. For

practical reasons, TTFD was administered twice daily for two months in the form

of rectal suppositories, each containing 50 mg of TTFD. Symptomatic responses

were determined through the use of the computer assessed Autism Treatment

Evaluation Checklist (ATEC) forms. The erythrocyte transketolase (TKA) and

thiamine pyrophosphate effect (TPPE), were measured at outset and on completion

of the study to document intracellular thiamine deficiency. Urines from patients

were examined at outset, after 30 days and after 60 days of treatment and the

concentrations of SH-reactive metals, total protein, sulfate, sulfite,

thiosulfate and thiocyanate were determined. The concentrations of metals in

hair were also determined. RESULTS: At the beginning of the study thiamine

deficiency was observed in 3 out of the 10 patients. Out of 10 patients, 6 had

initial urine samples containing arsenic in greater concentration than healthy

controls. Traces of mercury were seen in urines from all of these autistic

children. Following administration of TTFD an increase in cadmium was seen in 2

children and in lead in one child. Nickel was increased in the urine of one

patient during treatment. Sulfur metabolites in urine did not differ from those

measured in healthy children. CONCLUSIONS: Thiamine tetrahydrofurfuryl disulfide

appears to have a beneficial clinical effect on some autistic children, since 8

of the 10 children improved clinically. We obtained evidence of an association

of this increasingly occurring disease with presence of urinary SH-reactive

metals, arsenic in particular.

Publication Types:

Clinical Trial

PMID: 12195231 [PubMed - indexed for MEDLINE]

1: Toxicology. 2005 Mar 30;208(3):357-65.

The effects of gestational arsenic exposure and dietary selenium deficiency on

selenium and selenoenzymes in maternal and fetal tissues in mice.

Miyazaki K, Watanabe C, Mori K, Yoshida K, Ohtsuka R.

Department of Public Health, Division of Environmental Medicine, Gunma

University Graduate School of Medicine, 3-39-22, Showa-machi, Maebashi City,

Gunma 371-8510, Japan.

Although toxicological and metabolic interactions of arsenic (As) and selenium

(Se) have been suggested by epidemiolgical literatures, the past experimental

studies mostly focused on acute, high-dose interaction, leaving the long-term,

low-dose interaction unexplored. In the present study pregnant mice, fed either

Se-deficient or adequate (0 or 5mumolSe/kg diet, respectively) diet, were given

oral gavage of sodium arsenite (0 or 58mumol/kg per day; chosen as less than

half of the fetotoxic dose in this protocol) from gestational day (GD) 7-16. The

levels of As and Se as well as five selenoenzymes (glutathione peroxidase (GPx),

thioredoxin reductase (TRxR), and type-I, -II and -III iodothyronine deiodinases

(DI-I, -II and -III) were examined on GD17 in the tissues of dams and of fetus.

The Se-deficient mice showed significantly enhanced accumulation of As compared

to the Se-adequate mice in maternal liver (increased by 48%) and fetal brain (by

31%). Although no direct evidence of the enhanced toxicity in the Se-deficient

group was obtained, the As exposure affected the levels of Se and selenoenzymes,

an effect which was more discernible in Se-deficient group. Although most of

theses changes were mild or moderate, the DI-II activity in Se-deficient fetal

brain showed a drastic four-fold increase by As exposure, suggesting a possible

disturbance of thyroid hormone environment in the fetus. These data suggested

that apparently non-toxic, in utero dose of As, showed enhanced accumulation

when combined with Se-deficiency and could affect the metabolism/kinetics of Se

in fetal brain, which might result in developmental toxicity in mice.

PMID: 15695021 [PubMed - in process]

2: Indian J Exp Biol. 2004 May;42(5):495-8.

Arsenic induced free radical toxicity in brain of mice.

Rao MV, Avani G.

Department of Zoology, University School of Sciences, Gujarat University,

Navrangpura, Ahmedabad 380 009, India. zooldeptgu@...

The present study was designed to investigate the in vivo effects of oral

administration of arsenic trioxide (As2O3; 0.5 and 1 mg/kg body weight/day for

45 days) on cerebral hemispheres and cerebellum in male mice, Mus musculus.

Arsenic reduced the concentration of glutathione (GSH) in cerebral hemisphere

and cerebellum at both the dose levels; while increased lipid peroxidation (LPO)

in cerebral hemisphere and cerebellum regions. Further, the activities of

antioxidant enzymes viz., superoxide dismutase and catalase also declined in

these two regions with dose indicating oxidative stress. This effect is caused

by the action of reactive oxygen species (ROS) induced by arsenic exposure.

PMID: 15233475 [PubMed - indexed for MEDLINE]

3: Neurotoxicology. 2003 Aug;24(4-5):747-53.

The effects of chronic arsenic exposure from drinking water on the

neurobehavioral development in adolescence.

Tsai SY, Chou HY, The HW, Chen CM, Chen CJ.

Department of Neurology, Tzu-Ai General Hospital, 321-90 Shin-Sur, Shilo,

Yunlin, Taiwan. sytsai@...

This cross-sectional study examined the possible influence on the development of

cognitive function among adolescents due to long-term arsenic exposure.

Forty-nine junior school students drinking arsenic-containing well water and 60

controls matched with age, sex, education, body height, body weight, body mass

index, and socioeconomic status were compared. The former was divided into two

groups: high and low exposure, with mean cumulative arsenic levels of

520629.0+/-605824.2 and 13782.2+/-12886.0 ppm, respectively. Four

neurobehavioral tests including continuous performance test (CPT), symbol digit

(SD), pattern memory (PM) and switching attention (SA) were applied. A strong

correlation between age and education caused collinearity in the multiple

regression model (r=0.84, P<0.0001). Only education and sex, excluding age, were

entered into the model as covariates. Pattern memory and switching attention

were significantly affected by long-term cumulative exposure to arsenic after

adjusting for education and sex. It is suggested that the arsenic levels in the

well water may be monitored extensively, but if there is no intervention, then

neurobehavioral function will not be protected. Limitations of the current study

require replication of this effect in other studies to confirm this conclusion.

PMID: 12900089 [PubMed - indexed for MEDLINE]

4: Toxicol Lett. 2002 Mar 10;128(1-3):73-84.

Arsenic induced changes in growth development and apoptosis in neonatal and

adult brain cells in vivo and in tissue culture.

Chattopadhyay S, Bhaumik S, Nag Chaudhury A, Das Gupta S.

Department of Life Science and Biotechnology, Jadavpur University, Kolkata

700032, India. c_sukumar@...

Arsenic at a nonlethal level in drinking water consumed over a period of time

has been reported to produce chronic toxicity and various types of health

problems ranging from skin cancer to disturbance in memory. Neurotoxic effects

have been reported in clinical cases with chronic exposure to arsenic.

Physiological detoxication of arsenic occurs partially through methylation.

Arsenic and its methylated derivatives are distributed in different organs and

systems. The present study examined the possible interference in the neuronal

development and differentiation due to the exposure to arsenic during gestation.

The experiments were carried out to examine short and long term effects of

arsenic on brain explants and cells grown and maintained in tissue culture

system. The effects of arsenic exposure showed changes in brain cell membrane

function indicated by generation and release of reactive oxygen-nitrogen

intermediates. On the morphological aspect the explants' growth was reduced,

ground matrix was lost and neural networking was inhibited. Cells showed signs

of apoptotic changes. Arsenic toxicity may induce damage to brain cells prior to

more visible clinical conditions. The deleterious effects also pass from the

maternal to fetal tissue across the transplacental barrier.

PMID: 11869819 [PubMed - indexed for MEDLINE]

5: Toxicol Appl Pharmacol. 2001 Jul 15;174(2):130-8.

Arsenic induces apoptosis in rat cerebellar neurons via activation of JNK3 and

p38 MAP kinases.

Namgung U, Xia Z.

Department of Environmental Health, University of Washington, Seattle,

Washington 98195-7234, USA.

Primary cultures of rat cerebellar neurons were used to study mechanisms of

arsenic neurotoxicity. Exposure to 5, 10, or 15 microM sodium arsenite reduced

cerebellar neuron viability and induced nuclear fragmentation and condensation

as well as DNA degradation to oligonucleosome fragments. Exposure to 1 or 5 mM

dimethylarsinic acid caused similar changes. Therefore, both inorganic arsenite

and organic dimethylarsinic acid induce apoptosis in cerebellar neurons, with

the inorganic form being more toxic. Cotreatment with cycloheximide or

actinomycin D, inhibitors of protein or RNA synthesis, respectively, or with the

caspase inhibitor zVAD, completely blocked arsenite-induced cerebellar neuron

apoptosis. This implies that arsenite-induced cerebellar neuron apoptosis

requires new gene expression and caspase activation. Interestingly, sodium

arsenite selectively activated p38 and JNK3, but not JNK1 or JNK2 in cerebellar

neurons. Blocking the p38 or JNK signaling pathways using the inhibitors

SB203580 or CEP-1347 protected cerebellar neurons against arsenite-induced

apoptosis. These data suggest that arsenite neurotoxicity may be due to

apoptosis caused by activation of p38 and JNK3 MAP kinases. Copyright 2001

Academic Press.

PMID: 11446828 [PubMed - indexed for MEDLINE]

6: Neurotoxicology. 2000 Aug;21(4):475-87.

Neurological effects of environmental exposure to arsenic in dust and soil among

humans.

Gerr F, Letz R, PB, Green RC.

Department of Environmental and Occupational Health, Rollins School of Public

Health, Emory University, Atlanta, GA 30322, USA. fgerr@...

Persons living in a small town in Georgia, USA, were studied because of known

environmental exposure to arsenic-containing dust. To assess the effects of this

exposure on the nervous system, a cross-sectional epidemiological study was

performed. The health outcome assessments of the study were based on a priori

selected clinical examination results and quantitative electrophysiologic and

behavioral outcome measures. Because the primary goal was to identify cases of

peripheral neuropathy, a clinically relevant case definition, based on results

of these outcomes was created. Historical exposure reconstructions were

performed on a subset of the exposed subjects for whom such information was

available. Of the 238 persons enrolled in the study, 133 were classified as

non-exposed (i.e., did not reside in the area of known exposure) and 105 were

classified as exposed (i.e., did reside in the area of known exposure).

Following exclusions of persons with occupational exposure to neurotoxicants,

pre-existing conditions associated with peripheral nerve impairment, or age

below 18 years, 118 unexposed subjects and 85 exposed subjects were available

for inclusion in the analyses of peripheral nerve outcomes. A total of 4 (3.4%)

of the unexposed subjects and 13 (15.3%) of the exposed subjects met the case

definitions for peripheral neuropathy (OR=5.1; p=0.004). Comparison of three

exposure groups (none, low, high) did not yield statistically significant

differences. Statistically significant exposure group differences were observed

on quantitative tests of standing steadiness, vibrotactile threshold and tremor

intensity but not for nerve conduction measures. These results demonstrate a

strong association between community arsenic containing dust exposure and

peripheral neuropathy among participants in this investigation.

Publication Types:

Clinical Trial

PMID: 11022857 [PubMed - indexed for MEDLINE]

7: Neurotoxicol Teratol. 1997 Nov-Dec;19(6):489-97.

Effects of lead-arsenic combined exposure on central monoaminergic systems.

Mejia JJ, -Barriga F, Calderon J, Rios C, Jimenez-Capdeville ME.

Departamento de Biologia Celular, Facultad de Medicina, Universidad Autonoma de

San Potosi, Mexico, USA.

Lead acetate (116 mg/kg/day), arsenic (11 or 13.8 mg/kg/day as sodium arsenite),

a lead-arsenic mixture or vehicle were administered to adult mice through

gastric intubation during 14 days. Then, the regional content of norepinephrine

(NE), dopamine (DA), serotonin (5-HT), 3,4 dihydroxyphenyl-acetic acid (DOPAC),

5-hydroxyindole-3-acetic acid (5-HIAA), arsenic, and lead were quantified.

Compared with the accumulation after single element exposures, the mixture

elicited a higher accumulation of lead and a lower arsenic accumulation in the

brain. Compared to controls, lead induced only an augmentation of DOPAC (200%)

in the hypothalamus. By contrast, the mixture provoked increases of DOPAC in the

hypothalamus (250%), DA and 5-HIAA in the striatum (67 and 187%, respectively)

and NE decreased in the hypothalamus (45%). Although these alterations were

similar to those produced by arsenic alone, the mixture provoked a 38% decrease

of NE in the hippocampus and increases of 5-HT in midbrain and frontal cortex

(100 and 90%, respectively) over control values, alterations that were not

elicited by either metal alone. These results demonstrate an interaction

arsenic/lead on the central monoaminergic systems of the adult mouse.

PMID: 9392784 [PubMed - indexed for MEDLINE]

8: Toxicol Lett. 1997 Aug 22;92(3):201-8.

Arsenic-induced changes in certain neurotransmitter levels and their recoveries

following chelation in rat whole brain.

Tripathi N, Kannan GM, Pant BP, Jaiswal DK, Malhotra PR, Flora SJ.

Divison of Pharmacology and Toxicology, Defence Research and Development

Establishment, Gwalior, India.

Arsenic as sodium arsenite (100 ppm in drinking water) was administered to male

rats for 16 weeks. Animals were then treated either with

meso-2,3-dimercaptosuccinic acid (DMSA), sodium 2,3-dimercaptopropane

1-sulfonate (DMPS), dimethyl DMSA (DmDMSA), or diisopropyl DMSA (DiPDMSA) twice

daily (50 mg/kg) intraperitoneally for 5 days. After 5 days of rest period, the

animals were again given a second course of chelation therapy. The animals were

sacrificed subsequently for the determination of whole brain biogenic amines

levels, acetylcholinesterase (AChE), monoamine oxidase (MAO) and

delta-aminolevulinic acid dehydratase (ALAD) activities. A number of biochemical

parameters and arsenic concentrations in some tissues were also determined. The

results suggest a significant increase in brain arsenic concentration

accompanied by alterations in neurotransmitters levels following As(III)

exposure. Although chelation treatment was effective in reducing As burden, the

altered biochemical variables responded less favorably to chelation therapy. The

DMSA-diesters, particularly DiPDMSA, produced a more pronounced increase in

brain arsenic burden, as well as alterations in a few neurotransmitters. It can

be concluded that the lipophilic character of As antidotes may lead to

unfavorable results following intraperitoneal administration.

PMID: 9334831 [PubMed - indexed for MEDLINE]

*

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