Vission/Mission
NSTDA:
A Driving Force for National Science and Technology Capacity
VISION
A key partner in developing a knowledge-based society through the application of science and technology
MISSION
Research and development to strengthen Thailand's sustainable competitiveness, complemented by
technology transfer and the development of human resources and science and technology infrastructure,
with outcomes that have positive impacts on society and the economy.
CORE VALUES
NSTDA embraces five core values as guiding principles to ensure performance excellence and efficient
interaction within NSTDA.
NSTDA core values are:
N = Nation First
S = S & T Excellence
T = Teamwork
D = Deliverability
A = Accountability
Reverse Brain Drain Project
(RBD-NSTDA)
Special Conference
Cadmium in Food and Human Health &
Technologies for
Environmental Restoration and
Rehabilitation
Topland Hotel Convention Center
Phitsanulok, Thailand.
January 15-17, 2010
Cadmium conference
conference 2010
Welcome Message
Cadmium conference 2010
Message from the President of
Naresuan University
On behalf of Naresuan University, I am honored to welcome all
distinguished speakers, participants, and exhibitors to the
Reverse Brain Drain Project (RBD-NSTDA) Special Conference
on “Cadmium in Food and Human Health and Technologies for
Environmental Restoration and Rehabilitation” to be held on 1517 January 2010 in Phitsanulok.
This important event will allow researchers and scientists in the
fields of environmental health research, food safety and security,
and environmental management from various corners of the
world to gather and exchange their experiences and ideas on
research related to cadmium. Moreover, it will allow you to synthesize information and
research findings to better serve your fields of studies and professions. This conference will
also encourage discussion on how to minimize the entry of toxic heavy metals including
cadmium into the environment and food chain. Dr. Soisungwan Satarug, Overseas Thai
Professional Project Leader, has played a leadership role in enhancing concern for and
influence cadmium contamination, exposure, and toxicity in Thailand and throughout the
world.
I would like to thank the National Science and Technology Development Agency (NSTDA)
for their support for this specific conference. Many thanks also go to the organizing
committee who helped with organizing this important conference.
Finally, I wish this conference all success and that it will be a productive and enjoyable
experience for you all.
Sincerely,
Prof. Dr. Sujin Jinahyon
President, Naresuan University
Cadmium conference 2010
II
FOREWORD
It is most delightful to welcome you to a special conference of
the Thailand Reverse Brain Drain Project (RBD-NSTDA) on
Cadmium in Food and Human Health. This meeting has
received support from the Reverse Brain Drain Project of
National Science and Technology Development Agency,
Commission for Higher Education in co-operation with
Naresuan University and I am most grateful for this support. I
thank everyone for taking the time and making the effort to
travel (half-way around the world) to perhaps move out of your
comfort zone in order to contribute to this conference.
What we are going to examine together in two and a half days of this conference is a close
link between environmental quality and population health (environmental medicine).
Numerous epidemiological and toxicological studies over the last five years have brought
into light many adverse effects of chronic (long-term) environmental exposure to low-level
cadmium together with mechanistic plausibility of those effects observed. Among those,
cadmium toxicity has been demonstrated not only in the kidney and bone, but also in almost
every tissue and organ where its presence is detectable. With increasing evidence for the role
played by multiple metal transporters (zinc, iron, manganese transporters) in mediating
cellular cadmium influx and efflux, it becomes apparently clear that cadmium can enter into
any cells, expressing those transporters. Tissue-differential effects of cadmium can be
expected based on the expression patterns of various transporters among tissues with
differences in physiological function and their requirement for essential metals. This
conference draws your attention to an upward trend in food cadmium content and population
exposure levels. On the other hand, it is heartening that a reduction in cadmium exposure
from cigarette smoking has been reported in some countries. With the recognition of risk to
the environment and human health, the management of cadmium in the environment and in
agriculture will be increasingly important as will be the innovation of monitoring devices and
remediation strategies.
No scientific research is considered complete without communication of what has been found
in the enquiry. I would therefore like to invite/encourage you to submit your work presented
in this conference for consideration of publication in Toxicology Letters: 2010 Special Issue.
A dedicated website will be established through which submission should be made Your
paper will undergo peer review as in the standard code of practice of Journal. Instructions for
preparing a paper are available on http://ees.elsevier.com/toxlet/. As a member of the
Editorial Board and Guest Editor for the TL Special Issue, I look forward to receiving your
submission.
Once again, many thanks for your attending and participating in this conference. I
hope your experience proves to be worthwhile and perhaps even inspirational in your future
scientific endeavors.
Soisungwan Satarug, M.C.H (Nutrition), Ph.D. (Biochemistry)
Overseas-based RBD Project Leader,
Honorary Research Fellow, National Research Centre for Environmental Toxicology,
Brisbane, Queensland, Australia, Visiting Research Professor, Pathology Department,
University of North Dakota School of Medicine and Health Sciences, Grand Forks, ND
58202, USA.
Cadmium conference 2010
III
Message from the Dean of
Faculty of Medical Science, Naresuan University
On behalf of the organizing committee of the Reverse Brain Drain Project (RBD-NSTDA)
International Conference Cadmium in Food and Human Health &Technologies for
Environmental Restoration and Rehabilitation, it is my great pleasure to all speakers and
participants to attend this special conference at Phitsanulok on 15-17 January 2010.
The mission of Faculty of Medical Science, Naresuan University is to foster board
international scientific cooperation. Its aim is to promote acquisition, dissemination, and
utilization of knowledge of sciences. I hope that all participants will fully benefit from this
meeting.
I would like to thanks to the National Science and Technology Development Agency
(NSTDA) and the organizing committee on organizing the conference.
Besides the excellent program, all participants will enjoy the warm hospitality during the
conference.
Sincerely,
Assoc. Prof. Dr. Rosarin Wongwilairat
Dean, Faculty of Medical Science,
Naresuan University
Cadmium conference 2010
IV
Welcome Message
On behalf of the Graduate School, Naresuan University, it is my great pleasure to welcome
you to the Thailand Reverse Brain Drain Project International Conference on Cadmium in
Food and Health, Naresuan University, and our lively Phitsanulok Province.
In this conference, we are certain that there will be of great benefit for participants in
gathering new knowledge and experiences through presentations, discussions, and idea
exchange during this 3 – day meeting. We also hope for new networks to be built from us in
this conference. We believe that such networks will strengthen our research resulting in the
advancement of knowledge in the field. It is our expectation that such advance knowledge
would be beneficial to good health and good quality of life of people worldwide.
I would like to express my sincere gratitude to our guest speakers, participants, all sponsors
and honorary guests for making this conference realized.
Finally, I would like to thank the organizing committee and staff members for their hard
working that make this conference very successful.
Kanungnit Pupatwibul, Ph.D
Dean
Graduate School
Naresuan University
Cadmium conference 2010
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Thailand-based, Co-leader
Dear Conference Participants,
On behalf of the Organizing Committee, it gives me great
pleasure to welcome you to the Reverse Brain Drain Project
(RBD-NSTDA) Special Conference on “Cadmium in Food and
Human Health &Technologies for Environmental Restoration and
Rehabilitation”. I remembered that this research group on
cadmium was started as a session in the International Conference
organized by the Faculty of Medical Science a few years back.
Now, with our tireless effort, we are hosting a conference on
cadmium research here at Naresuan University. It is indeed a
successful effort to have prominent scientists from several parts
of the world to form research networks with our faculty members
and staff. Till today the cadmium research group at Naresuan
University has flourished and has several active faculty members recruiting many
undergraduate and graduate students. I do believe our participants will learn a great deal from
these excellent scientists. This is very exciting times to all of us that we are being offered the
opportunities to unveil challenging tasks at hand. Therefore, it is critical to encourage
constructive thinking and public discussion at this conference, as well as to ensure that our
scientists continue their research to bring the excellence to our communities and society.
Personally, I would like to thank the National Science and Technology Development Agency
(NSTDA), the Reverse Brain Drain Project, and those invited speakers to agree to come and
share their knowledge and experience, and thank you all the staff of the Faculty of Medical
Science, Naresuan University to make this conference happen. I do wish every participant
received outcome beyond your expectations.
Assoc. Prof. Dr. Sukkid Yasothornsrikul
Associate Dean for Research and Graduate Studies
Faculty of Medical Science, Naresuan University
Cadmium conference 2010
VI
Introduction of the conference
Environmental health education and research in Thailand is limited. This has in part resulted
from a lack of a critical mass of Thailand-based researchers with experiences in assessment
of environmental exposure to heavy metals and its impact on population health, food
production system and wildlife. This situation places Thailand in a vulnerable position as
being the world leading food export. This conference is a step towards enhancement of
research and research training in Thailand in the area of Environmental Health along with the
sensor technological innovation for on-site use in monitoring of environmental pollution.
This conference receives initial support from the Reverse Brain Drain/National Science and
Technology Development Agency (NSTDA) and the Commission for Higher Education
(CHE).
Reverse Brain Drain Project (RBD-NSTDA) Special Conference Cadmium in Food and
Human Health &Technologies for Environmental Restoration and Rehabilitation will cover
three main themes; Health Effects, Case Studies, and Management & Risk Minimization. It is
designed to be inclusive and thus it will consider also other toxic metals of local concerns
which may include lead and mercury. All interest individuals are encouraged to participate.
Thai to English translation will also be made available to enhance information exchange on
local environmental health issues.
Cadmium conference 2010
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GENERAL INFORMATION FOR THE CONFERENCE
PHITSANULOK, THAILAND
Covering some 105,815 square kilometers, Phitsanulok is 377 kilometers
north of Bangkok. It borders Uttaradit Province on the North, Phichit
Province on the South, Loei and Phetchabun Provinces on the East, and
Kamphaeng Phet and Sukhothai Provinces on the West. Situated on a
strategic location dividing Thailands Central and Northern regions, and
connecting to the Northeastern region, Phitsanulok is undeniably an
important hub and an ideal base for travelers wishing to explore the lower
North and western Northeast. Phitsanulok, however, is not just a stopover
for tourists, but is a province with promising tourism opportunities.
Phitsanulok City spans the banks of Maenam Nan and has Maenam
Kwae Noi running through it. Therefore, it is locally known and
historically referred to as Song Kwae City (song means two and kwae means a river). Most of
Phitsanulok's terrain is flatlands, with one third of the area being mountain ranges on the
north and the east. Its unique natural endowments including natural parks and waterfalls
make a trip to Phitsanulok worthwhile.
Apart from its exceptional natural charisma, Phitsanulok
provides visitors with an opportunity to explore notable chapters of Thailand's history. For
example, remains of an ancient community dating back between 2,000-4,000 years, including
old stone axes, was found here. In addition, the old temple of Wat Chula Mani, situated 5
kilometers south of the city, was built even before the Sukhothai Kingdom burst into power.
Phitsanulok prospered along with the powerful Sukhothai (1238-1378) and Ayutthaya (1350
1767) Kingdoms. In particular, it played a strategic role in the Ayutthaya era when it had
become the Kingdoms royal capital for 25 years during the reign of King Borom Trailokanat.
Phitsanulok is also the birthplace of King Naresuan the Great
(reigned 1590-1605) the
legendary King who declared Ayutthayas independence from Burma in 1584. King Naresuan
the Great is known for his victorious and honorable single hand combat on elephant back
Yutthahatti against a Burmese Crown Prince. His heroic power and strong dedication to
expelling the invaders from his motherland saved the country, and truly united the Kingdom
which later was known as Siam and currently known as Thailand.
Phitsanulok was also a strategic location for other Ayutthaya Kings as it was a major center
for military recruitment and a training camp when Ayutthaya waged wars with Burma.
Cadmium conference 2010
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VENUE
Topland Hotel
68/33 Akathodsarod St. A.Muang Phitsanulok THAILAND 65000
Tel. +66-55 247800-9, 245390-4 Fax. +66-55 247815, 245395
E-mail : phsoffice@toplandhotel.com
Directions
The distance from Phitsanulok International Airport (PHS) to the hotel is 7 kilometres
and takes 15 minutes by car.
Cadmium conference 2010
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TRANSPORTATION
Phitsanulok is located in the lower-northern part of Thailand, about 377 kms from Bangkok.
There are three ways to get to Phitsanulok from Bangkok:
1. By train-approximately 6.30 hrs (http://www.railway.co.th/english/index.asp)
2. By bus-approximately 5.30 hrs (http://www.transport.co.th)
3. By plane-approximately 45 mins (www.thaiairways.com)
The most common way for people to travel around Phitsanulok is city bus. Drive form the
conference hotel to downtown will generally cost 10-15 Bath. Tuk Tuk (three wheels taxi)
are also available in front of the conference hotel just tell the driver your destination. It is
recommended that you negotiate a price before commencing your trip.
PHONE
The numbers to call for Fire, Police and Ambulance. Also drug help, poisons and emergency
doctors, hospitals and blood transfusion services. Plus Consular contacts: where to call if you
need your country’s help.
Emergency Services
Telephone
Tourist Police
1155
Police (General Emergency Call)
191
Ambulance and Rescue
1554
Fire
199
National Disaster Warning Centre
1860
Crime
1195
Medical Emergency Call
1669
Organization of the conference
…………………………………………………………………………
Organizers
National Science and Technology Development Agency (NSTDA)
Commission for Higher Education (CHE)
Naresuan University
Faculty of Medical Science, Naresuan University
Graduate School, Naresuan University
…………………………………………………………………………
Cadmium conference 2010
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Organizing Committee Advisory Board
Prof. Dr. Sujin Jinayon
Assoc. Prof. Dr. Sakarindr Bhumiratana, President of National Science and Technology
Development Agency (NSTDA)
Dr. Noppawan Tanpipat Assistant President of National Science and Technology
Development Agency (NSTDA)
Dr. Sumet Yamnoon, Commission Secretary-General of Commission on Higher Education
(CHE)
Prof. Dr. Kanchana Ngourungsi
Prof. Dr. Wisaka Limwongse
Prof. Dr. Keith J. Syer
Prof. Taweesook Kanluan
Asst. Prof. Dr. Kanungnit Pupatwibul
Assoc. Prof. Dr. Rosarin Wongwilairat
…………………………………………………………………………
International Scientific Program Committee
Prof. Dr. Soisungwan Satarug
Prof. Dr. Donald A. Sens
Prof. Dr. Mary Ann Sens
Prof. Dr. Marie Vahter
Dr. Michael Warne
…………………………………………………………………………
Local Organizing Committee
Assoc. Prof. Dr. Sukkid Yasothornsrikul
Dr. Wisa Supanpaiboon
Asst. Prof. Wiphawi Hipkaeo
Asst. Prof. Tantip Boonsong
Dr. Natthiya Sakulsak
Dr. Chanchira Wasuntarawat
Dr. Supaporn Puntheeranurak
Dr Watcharee Tiangyou
Dr. Onrawee Khongsombat
Dr Piyarat Srisawang
Dr Wachirawadee Malakul
Mr. Yutthapong Tongpob
Mr. Sangkab Sudsaward
Miss Tippaporn Bualeong
Miss Laorrat Phuapittayalert
Miss Keerakarn Somsuan
Mr Pisid Seang-Ananta Karn
Mr. Sucha Noomkleng
Mr. Thongchai Norkaew
Miss Nuchareeporn Thongrod
Miss Sutankamol Krongyut
…………………………………………………………………………
Cadmium conference 2010
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Reverse Brain Drain Project (RBD(RBD-NSTDA)
Special Conference
Cadmium in Food and Human Health &Technologies
for Environmental Restoration and Rehabilitation
Convention Hall 2, Topland Hotel Convention Center
Phitsanulok, January 1515-17, 2010
January 15, 2010
Presentation Topic/Speaker
8:00-9.00
Registration
Setting and Putting up Posters
Opening Ceremony
Keynote lecture:
Dr Sujin Jinayon, President of Naresuan University, Thailand
Plenary Lecture:
Cadmium, Dietary Exposure and Health Effects-An Overview
Dr Soisungwan Satarug, University of North Dakota, USA
Coffee Break
Chairperson: Dr Kanungnit Pupatwibul
S1-1
Chronic Renal Failure in Sri Lanka Caused by Elevated Dietary
Cadmium:Trojan Horse of Green Revolution
Dr Sarath Bandara, University of Peradeniya, Peradeniya, Sri Lanka
S1-2
Estimation of Benchmark Dose for Cadmium-induced Renal Effects in
Humans
Dr Yasushi Suwazono , Chiba University, Japan
Questions and Discussion
Lunch
Chairperson: TBA
S2-1
Lead, Cadmium and Arsenic Interactions at LOEL Dose Levels- An
Overview
Dr Bruce Fowler, ATSDR, USA
S2-2
Mitochondria, Reactive Oxygen Species and Cadmium Toxicity
Dr Glenda Gobe, University of Queensland, Australia
S2-3
Cadmium-induced Apoptosis Signaling in Cultured Kidney Proximal Tubule
Cells
Dr Frank Thévenod, University of Witten/Herdecke, Germany
S2-4
Microsatellite Markers of Immune Responses Gene as a Tool for
Immunogenetic Analysis of Parasitological Disease
Dr Mihoko Kikuchi, Nagasaki University, Japan
Questions and Discussions
Coffee Break
Poster viewing
Welcome Reception
9.00-9.15
9:15-9:45
9:45-10.15
10:15-10:45
Session 1
10:45-11.15
11:15-11:45
11.45-12.00
12:00-13:00
Session 2
13:00-13:30
13:30-14:00
14.00-14.30
14:30-15:00
15.00-15.15
15.15-15.30
15.30-16.30
18.30-21.30
January 16, 2010
Presentation Topic/Speaker
Session 3
8:40-9:10
Chairperson: Dr Soisungwan Satarug
S3-1
Naturally Exposed Animal Populations as a Bio-indicator of Environmental
Pollution by Cadmium
Dr Wisa Supanpaiboon, Naresuan University, Thailand
S3-2
Cadmium-induced Toxicity in Bank Voles (Bandicota indica) from Highversus Low-Exposure Areas
Dr Wiphawi Hipkaeo, Naresuan University, Thailand
S3-3
Essential Metals and Cadmium Toxicity in the Kidney
Dr David Vesey, University of Queensland, Australia
Questions and Discussions
Coffee Break
Chairperson: TBA
S4-1
Maternal and Early-life Cadmium Exposure in Rural Bangladesh
Dr Marie Vahter, Institute of Environmental Medicine, Karolinska Institutet,
Sweden
S4-2
Cadmium and Age-related Macular Degeneration
Dr Nilesh M. Kalariya, University of Texas Medical Branch, USA
Questions and Discussions
Lunch
Chairperson: Dr Sukkid Yasothornsrikul
S5-1
Environmental Cadmium Exposure and Oral disease
Dr Manish Arora, Harvard School of Public Health, USA and
University of Sydney, Australia
S5-2
Cadmium Carcinogenesis: Lessons from Renal Toxicity Studies
Dr Frank Thévenod, University of Witten/Herdecke, Germany
S5-3
Molecular Biology of Nickel Carcinogenesis
Dr Joseph Landolph, University of Southern California, USA
Coffee Break
Oral Short Communication
DMSA Alleviates Oxidative Stress and Vascular Dysfunction in Mice with
Long-term Exposure to Cadmium
Ms Kwanjit Sompamit, Mahasarakham University, Thailand
Poster viewing
9:10-9:40
9:40-10:10
10:10-10:30
10.30-10.45
Session 4
10.45-11.15
11:15-11:45
10:45-12:00
12.00-13.00
Session 5
13:00-13:30
13:30-14:00
14:00-14:30
14:30-15:00
15.00-15.20
15:20-16:30
January 17, 2010
Presentation Topic/Speaker
Session 6
8:45-9:15
Chairperson: Dr Kieth Syers
S6-1
International Food Legislation (Dr Soisungwan Satarug)
S6-2
NHANES Cadmium Biomonitoring Studies in the General U.S. Population –
An Overview
Dr Bruce Fowler, ATSDR, USA
S6-3
Research Into and Management of Cadmium in Australian Agriculture
Dr Michael Warne, Australia
Questions and Discussions
Coffee Break
Chairperson: Dr Soisungwan Satarug
S7-1
Bioremediation of Cadmium Contaminated Irrigation and Drinking Water: A
Large Scale Approach
Dr Sarath Bandara, University of Peradeniya, Peradeniya, Sri Lanka
S7-2
A Study of Cadmium in Soils and Vietnamese Standard of Cadmium in
Agricultural Soils
Dr Pham Quang Ha Institute for Agricultural Environment (IAE/VAAS),
Vietnam
Questions and Discussions
Best Poster Awards and Closing Ceremony
Lunch
Excursion: Sukhothai Historical Park
9:15-9:45
9:45-10:15
10:15-10:30
10:30-10:45
Session 7
11:15-11:45
10:45-11:15
11:45-12:00
12:00-12:15
12:15-13:15
13:30-17:00
Cadmium conference 2010
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Reverse Brain Drain Project (RBD(RBD-NSTDA) Special Lecture on
Cadmium in Food and Human Health:
Technologies for Environmental Restoration and Rehabilitation
Monday, 18 January 2010
09.30 – 15.00
Room 110 (Theater), 1st floor Central Building
National
National Science and Technology Development Agency (NSTDA)
Thailand Science Park, Pathumthani
09.00 – 09.30
09.30 – 09.40
09.40 – 11.45
Registration (in front of room 110)
Welcome and introduction
Dr.Noppawan Tanpipat, Assistant President of NSTDA
- Executive summary: Why monitoring of environmental pollution by
cadmium?
- Cadmium detection: on-site sensor, biosensor development?
Dr. Soisungwan Satarug
Visiting Research Professor, University of North Dakota School of
Medicine and Health Sciences, USA
Honorary Research Fellow, the National Research Centre for
Environmental Toxicology, Brisbane, Queensland, Australia
- Why we need quality assurance quality control and inter-laboratory
accreditation programs for cadmium analysis in soil and plants?
- The Australian National Cadmium Minimisation Strategy - an
integrated approach to address cadmium in Australian agriculture.
Dr. Michael Warne, Land and water, CSIRO, Australia
- Clean up: Sri Lankan experiences
- Bio-remediation of cadmium contaminated irrigation and drinking
water:
A large scale approach.
Dr. Sarath Bandara, the University of Peradeniya, Sri Lanka
- Monitoring: Swedish experiences
- Environmental exposure to cadmium in Sweden
Dr. Marie Vahter, Institute of Environmental Medicine (IMM),
Karolinska Institutet, Sweden
- Monitoring: US experiences
- The National Health and Nutrition Examination Survey (NHANES)
biomonitoring studies
Dr. Bruce Fowler, Agency for Toxic substances and Disease Registry,
Centers of Disease Control and Prevention, Atlanta, USA
- Cadmium in soils and Vietnamese standard of cadmium in phosphate
fertilizers and agricultural soils
Dr. Pham Quang Ha, National Institute for Soils and Fertilizers,
Hanoi, Vietnam
11.45 – 12.30 Q&A
12.30 – 13.30 Lunch at room 101 (Board room)
13.30 – 15.00 Round-table discussion at room 101 (Board room)
Cadmium conference 2010
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ABSTRACTS
Cadmium conference 2010
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NARESUAN UNIVERSITY
Reverse Brain Drain Project (RBD-NSTDA)
Special Conference
Cadmium in Food and Human Health &Technologies for
Environmental Restoration and Rehabilitation
Keynote lecture
Prof Dr Sujin Jinayon,
President of Naresuan University
Phitsanulok Thailand
Cadmium conference 2010
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Cadmium, Dietary Exposure and Health
EffectsEffects-An Overview
Soisungwan Satarug*,1 ,2, Scott H. Garrett2, Mary Ann Sens2 and Donald A. Sens2
*
Honorary Research Fellow, 1National Research Centre for Environmental Toxicology, Brisbane, Queensland,
Australia, 2Visiting Research Professor, Pathology Department, University of North Dakota School of Medicine
and Health Sciences, Grand Forks, ND 58202, USA.
Cadmium appears as a contaminant in most human foodstuffs because of its high rates of soilto-plant transfer, rendering diet a primary source of exposure among non-smoking, nonoccupationally exposed populations. Bioavailability of ingested cadmium has been shown among
high consumers of the food high in cadmium such as oysters, oilseeds and offal. The bioavailability
of cadmium of the dietary origin is further strengthened by the substantial amounts of cadmium
accumulation in kidneys, eyes and other tissues and organs of individuals without exposure in the
workplace or smoking of cigarettes. It is hypothesized that such accumulation results from the
efficient absorption and systemic transport of cadmium, employing multiple transporters that are used
for the body’s acquisition of calcium, iron, zinc and manganese. Adverse effects of cadmium on
kidney and bone have been observed in environmentally exposed populations at the frequencies
higher than those predicted from models of exposure. There is increasing evidence implicating
exposure to cadmium in the risk of diseases that involve other tissues and organ systems at very low
cadmium levels not producing any observable effects on bone or renal function. Long-term exposure
to high-dose cadmium is known to cause the Itai-itai disease. This disease affects mainly women and
is characterized by severely impaired tubular and glomerular function, generalized osteomalacia and
osteoporosis with resultant multiple bone fractures. An estimate of cadmium intake, based on historic
rice cadmium content, in the Itai-itai disease endemic area during 1960s was 600 µg/day and the
threshold lifetime intake was estimated to be between 1580 and 2000 mg of cadmium. Long-term
exposure to low-dose cadmium has been linked to tubular impairment with a loss of re-absorptive
capacity for nutrients, vitamins and minerals. These loses include zinc and copper bound to the metal
binding protein metallothionein (MT), glucose, amino acids, phosphate, calcium, β2-MG, retinolbinding protein (RBP) and vitamin D binding protein. There is compelling evidence linking tubular
impairment with urinary calcium loss, rapid bone demineralization and osteoporosis. Mild tubular
impairment and renal injury have been found associated with increased risk of high blood pressure
levels. Current data links low levels cadmium exposure also with diabetes, diabetic nephropathy,
hypertension, peripheral arterial disease (PAD), myocardial infarction, diminished lung
function, periodontal disease and age-related macular degeneration (AMD).
Of particularly health concern is that cadmium is classified as a cancer causing agent in
humans by the International Agency for Research on Cancer, based on an elevated incidence of lung
cancer and mortality data derived from the occupational groups with evidence of elevated exposure to
cadmium. The occupational exposures have historically been through inhalation of cadmium. A
consequence of this initial association of inhaled cadmium with cancer in occupationally exposed
workers is that a carcinogenic risk from exposure to dietary origin has received little attention.
However, there is accumulating evidence linking elevated dietary exposure and increased cancer
incidence. Excess cancer mortality was found associated with environmental exposure to cadmium in
Japan and the US prospective studies. Increased endometrial cancer risk was observed in a Swedish
cohort among those consumed cadmium above 15µg/day, mainly from cereals and vegetables.
Evidence from prospective studies revealed potential causal relationships between cadmium exposure
and life-prognosis (all-cause mortality) and excess cancer mortality among US men. To date,
cadmium-cancer association has been observed for the lung, liver pancreas, breast, endometrium,
prostate and urinary bladder. These epidemiologic data argue strongly for public health measures for
reducing exposure from all sources including dietary, cigarette smoking and possibly polluted air
from which 50-60% of inhaled cadmium could be absorbed into systemic circulation. With the
looming cancer and chronic disease epidemic worldwide, we encourage consideration given to
cadmium exposure assessment, identification of potential exposure sources and determinant of
cadmium body burden in future epidemiologic investigations to allow an estimate of total disease
burden (cost) of the population exposure. There is a lack of therapeutically-effective chelating agents
to enhance excretion of cadmium and this factor makes prevention of cadmium accumulation pivotal.
The persistence of cadmium in the environment requires a long-term approach to minimize the foodchain transfer of cadmium and human exposure through environmental management and maintenance
of lower cadmium levels wherever possible.
Cadmium conference 2010
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SESSIONS 1
Cadmium conference 2010
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Chronic Renal Failure in Sri Lanka Caused by Elevated
Dietary Cadmium:Trojan Horse of Green Revolution
J.M.R.S. Bandara1, 2, H.V.P.Wijewardena2, J. Liyanege3 , M.A.Upul3 and J.M.U.A.Bandara4
1. Department of Agric. Biology, University of Peradeniya, Peradeniya, Sri Lanka.
2. Board of Study in Plant Protection, PGIA, University of Peradeniya, Peradeniya.
3. Department of Chemistry, University of Kelaniya, Kelaniya, Sri Lanka,
4. Pediatrics Ward, Teaching Hospital, Peradeniya.
Correspondence Author: bandara.sarath@gmail.com
An endemic form of CRF emerged in 2002 in the major farming provinces of Sri Lanka.
Though 2-3 % prevalence is reported in general the prevalence rate is more than 10% in North central
Province and North Western Province of Sri Lanka, the traditional farming areas of lowland rice. The
deaths reported due to CRF in hospitals in the affected provinces amounts to 300-600 annually,
though the total number of deaths due to CRF is 1400 per year. In the North Western Province where
the CRF is reported recently ,the death rate is 50-60 per year. Disease is common among lowland rice
cultivators and predominantly new occurrences are among the younger farmers with a male to female
ratio of 4:1. Elevated dietary Cadmium levels are the main factor identified. A PTWI of 15.47 – 28.39
of Cd µg/kg BW on a regular rice staple with Tilapia fish has been reported. The mean urinary
cadmium of inhabitants in the region affected with CRF is 7.58µg Cd/g creatinine (among confirmed
patients) – 11.6258µg Cd/g creatinine (among asymptomatic residents) indicated a chronic exposure
of the farmer population to Cd. The main source of cadmium that elevates the Cd level in food in
NCP must be identified for effective management of CRF. The mean cadmium contents in food items
collected from patients’ houses and their domestic environment including reservoirs of water revealed
that the dietary cadmium levels are influenced by both irrigation and drinking water resulting in
unusually higher levels of cadmium in all food items produced within the domestic environment. The
food items tested are rice staple, pulses , freshwater fish, lotus rhizomes, farm products especially
foliage vegetables, Cow’s milk, buffalo milk products and breast milk. The other sources of cadmium
tested are the agricultural soil, non agricultural soil, sediments in reservoirs and pasture.
Agrochemicals such as phosphate fertilizer and pesticides and surfactants used for pesticides were
also tested for Cd and Pb. The mean Cd levels in uncultivated soil in Anuradhapura district and
Polonnaruwa district of NCP are 0.023+ 0.014 and 0.0052 + 0.0043 mg/kg respectively. The mean Cd
content in cultivated soil applied with TSP in Anuradhapura is 0.1104 + 0.186 and in Polonnaruwa
0.0159 + 0.005 mg/kg. The soils of NCP are not naturally high in Cd but Cd is added to soil through
agricultural practices adopted. The NCP is the traditional agricultural area of Sri Lanka which
produced all her staple requirements in a sustainable manner during the ancient “Rajarata
Civilization” ( Rajarata = Ancient Kingdom) under man made irrigation system based on 4000 small
reservoirs arranged in 250 cascades during King Parakrama Bahu ( 1153-1186 AD). Though detailed
historical records of Sri Lanka are available in the Ancient Chronicle of Sri Lanka the, Mahawamsa
no records of epidemic or deaths due to chronic renal failure is reported. Irrigation system used today
in NCP is the renovated ancient irrigation system, which re-circulate drainage water from rice fields.
The main agrochemical that adds cadmium to agricultural field is the TSP or Rock Phosphates. The
Cd concentrations detected in TSP used in rice fields had a range from 23.50 -71.74 mg/kg. The use
of NPK fertilizer in rice cultivation increased with the introduction of new improved varieties with the
onset of Green Revolution in 1971. The quantum of fertilizer used with the use of high fertilizer
responsive rice varieties in 1975 is 74,000 Mt , more than double that was used in 1970 , a mere
32,000 Mt. Fertilizer use has increased tremendously with an annual growth rate of 3.5%. The
potential extreme level of Cd that could be in the rice- cascade reservoir environment since 1973 is
68.9 metric tons based on 71.74 mg Cd/kg TSP. We have determined the Cd content in several food
items including breast milk. The breast fed infants up to 2 years were subjected to heavy cadmium
intake with breast milk indicating possible involvement in occurrence of CRF among 9-12 years old
children. The trend in shifting the age of affected population towards younger farmers may be due to
early exposure to dietary cadmium even at breast feeding stage. We observed that further increase in
Cd in NCP occurred with the diversion of River Mahaweli for agricultural purpose in 1970-1980. The
average annual discharge from River Mahaweli is about 8.4 billion cubic meters which is used to
irrigate 140,000 ha in the NCP. We observed a range of 5-23 µg Cd/l of Mahaweli waters and
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specifically 10.8 µg of Cd/l at the first diversion canal at Polgolla. At an average flow of 6.679
million cubic meters per day at the rate of 10.8 µg of Cd/l, the potential transfer of cadmium from
Upper Mahaweli water to NCP from Polgolla alone is 72.13 kg/day. The total cadmium taken to
reservoirs along with the cadmium input generated from the irrigated TSP fertilized crop fields (rice
and vegetables) in the NCP eventually settled in the sediments of reservoirs (1.77 – 2.45 mg/kg). The
main source of Cd in tributaries of River Mahaweli is found to be from the TSP added to the
Catchment carrying high fertilizer responsive rice and vegetable plots and not the tea plantations that
use ERP.
Key Words: dietary cadmium, Chronic renal failure, TSP, Cd in breast milk, irrigation water and
cadmium
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Estimation of benchmark dose for CdCd-induced renal
effects in humans
humans
Yasushi Suwazono1, Mirei Uetani1 and Agneta Åkesson2
1
Department of Occupational and Environmental Medicine, Graduate School of Medicine, Chiba
University, 1-8-1 Inohana, Chuoku, Chiba 260-8670 Japan
2
Institute of Environmental Medicine, Karolinska Institutet,SE-171-77 Stockholm, Sweden
Correspondence author:suwa@faculty.chiba-u.jp
People are exposed to cadmium (Cd) via food and tobacco smoking. The first sign of renal
effects is a tubular damage, characterized by increased urinary excretion of low-molecular weight
proteins or intracellular tubular enzymes. In succession to the tubular effects, Cd may affect the
glomerular function. To protect people from Cd-induced health effects, it is crucial to determine the
reference exposure below which the probability of adverse health effects is low.
The benchmark dose (BMD) method, defined as the exposure that corresponds to a certain change in
response compared to the background, is increasingly used in the health risk assessment of
environmental contaminants. The lower 95% confidence bound of the benchmark dose (BMDL) has
been suggested to replace the no observed adverse effect level (NOAEL).
Recently, the BMD method has been applied to estimate the reference point of urinary Cd (U-Cd),
rice Cd concentration (R-Cd) and lifetime Cd intake (LCd) for renal effects.
In Swedish populations, BMDLs of U-Cd with BMR of 5% were 0.5 µg/g cre for tubular effect and
0.7 µg/g cre for glomerular effect.1 In Cd non-polluted area in Japan, BMDLs with BMR of 5% for
tubular effect were reported to be 0.3-0.7µg/g cre2 and 1.6-2.5µg/g cre.3 Furthermore, BMDLs of RCd with BMR of 5% for proteinuria with glucosuria were 0.18-0.27ppm4 and BMDLs of LCd with
BMR of 5% were 0.9-1.9g for tubular effect5 and 1.8-2.4g for proteinuria with glucosuria.6
These BMDLs of various Cd exposure index for renal effects were generally lower than expected
from earlier studies. Therefore, these results indicated the importance of further discussion for
comprehensive measures to decrease the Cd exposure in general population.
Keywords: Cadmium exposure; Urinary cadmium; Renal dysfunction; Benchmark dose; Dietary
cadmium; Cadmium body burden; Kidney toxicity
References
1.
Suwazono Y, Sand S, Vahter M, et al. Environ Health Perspect 2006;114:1072-6.
2.
Uno T, Kobayashi E, Suwazono Y, et al. Scand J Work Environ Health 2005;31:307-15.
3.
Kobayashi E, Suwazono Y, Uetani M, et al. J Appl Toxicol 2006;26:351-5.
4.
Kobayashi E, Suwazono Y, Dochi M, et al. Bull Environ Contam Toxicol 2009;83:102-7.
5.
Kobayashi E, Suwazono Y, Uetani M, et al. Bull Environ Contam Toxicol 2006;76:8-15.
6.
Kobayashi E, Suwazono Y, Dochi M, et al. Environ Toxicol 2009;24:421-8.
Cadmium
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SESSIONS 2
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Lead, Cadmium and Arsenic Interactions at LOEL Dose
LevelsLevels- An Overview
BA Fowler1, MH Whittaker2, G Wang3, X-Q Chen4, M Lipsky4, DSmith5, R Gwiazada5
ATSDR, Atlanta, GA, 2ToxServices, Washington, DC, 3Lovelace Respiratory Research Institute, Albuquerque
NM, 4Toxicology Program, Univ. Maryland, Baltimore, MD, 5 Environmental Toxicology Program, UCSC,
Santa Cruz, CA
1
Previous Pb, Cd, As interaction studies in rats (Fowler and Mahaffey, EHP 1978; Mahaffey
et al. J Lab Clin Med :, 1981) utilized a statistical factorial design to evaluate biological responses
produced by these elements incorporated into semi-purified diets at stressor dose levels for 10 weeks.
The present studies expanded this factorial design approach for examining interactions among these
elements using rats fed semi-purified diets but exposed to Pb, Cd, As in deionized drinking water at
Lowest Observed Effect Level (LOEL) dose levels for 30, 90 or 180 days, followed by evaluation of
molecular biomarker endpoints. The results of these studies demonstrated a number of additive
interactions which varied as a function of biomarker endpoint and duration of exposure. In general,
alterations in heme biosynthetic pathway parameters(ALAD, ZPP, urinary ALA, Kidney HSP32
mRNA) showed most pronounced effects at the 30 day, attenuation of effects at the 90 day and
increases at the 180 day time points. These responses were linked to a number of parameters of
oxidative stress, altered kidney concentrations of iron and copper and induction of cellular antioxidant
systems (GSH, metallothionein) which were most marked at the 90 day time point. At the 180 day
time point, a statistically significant increase in kidney 8OH-dG was observed in only the CdxAs
exposure group suggesting that this particular exposure combination produced DNA damage. The
overall results of these studies indicate that interactions among Pb, Cd, As occur at LOEL doses after
both short and long-term exposures but that the magnitude of these effects is dependent upon the
molecular endpoints measured, duration of exposure and the finite modifying effects of protective
antioxidant systems.
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Mitochondria, reactive oxygen species and cadmium
toxicity
Glenda Gobe.
Centre for Kidney Disease Research, University of Queensland School of Medicine, Princess Alexandra
Hospital, Woolloongabba, Brisbane, AUSTRALIA
Small intracellular organelles called mitochondria not only produce most of the energy for
cell metabolism, but they also produce reactive oxygen species (ROS). Normally, these ROS are
balanced by natural anti-oxidant enzymes, thereby negating any injury that might be caused by ROS.
When mitochondria are injured or become dysfunctional, for example, through long term exposure to
environmental toxins, they produce less cell energy and more ROS. The imbalance between these
ROS and the natural antioxidants creates a condition of oxidative stress, and this stress further injures
mitochondria, producing a vicious cycle of increasing injury. The heavy metal cadmium (Cd) is
known to accumulate in kidney cells, particularly those of the proximal tubular epithelium, and cause
oxidative stress. However, the molecular mechanisms accounting for Cd-induced oxidative stress are
not well-understood and the toxicity targets are largely unidentified. Mitochondria are key
intracellular targets for Cd. Our recent work has focused on the effects of cadmium on mitochondria
in kidney cells, particularly in relation to cell senescence and apoptosis. Renal proximal tubular cells
were treated with 10-5 to 10-7M cadmium chloride. Cells became either apoptotic or senescent
(TUNEL or beta-galactosidase) and lactate dehydrogenase levels increased (evidence of cell injury).
Specifically, mitochondria became swollen, rounded, and contained densities indicative of irreversible
cell injury (electron microscopy), autophagy of mitochondria increased (electron microscopy and
immunohistochemistry), the pro-apoptotic protein Bax, known to act at the mitochondrial membrane,
had increased expression (Western blot and immunohistochemistry), and mitochondrial membrane
potential was decreased (Mitotracker Red and confocal microscopy). Anti-oxidants, targeted to the
mitochondria, protected the cells somewhat from the cadmium toxicity. The outcome of such
mitochondrial injury is manyfold: injured mitochondria perpetuate a cycle of injury involving
continual oxidative stress; an attempt by cells to remove dysfunctional mitochondria through
autophagy leads to “autophagic cell death” or apoptosis; the loss of membrane potential causes release
of cytochrome-c, activating a caspase pathway leading to apoptosis and a gradual loss of functioning
renal cells; and decreased mitochondrial metabolism likely impacts on healthy levels of natural antioxidant enzymes. The three categories of mitochondrial regulation (upstream signaling pathways,
agents that target mitochondria directly, and downstream death-execution effectors) are all promising
as targets for effective treatment of cadmium toxicity.
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CadmiumCadmium-induced apoptosis signaling in cultured kidney
proximal tubule cells
Frank Thévenod1, Wing-Kee Lee1 and Blazej Torchalski1
1
Department of Physiology and Pathophysiology, University of Witten/Herdecke, Stockumer Str. 12,
D-58453 Witten, Germany
Correspondence author: frank.thevenod@uni-wh.de
The transition metal cadmium (Cd) is a significant environmental contaminant. Humans are
susceptible to Cd toxicity primarily through occupational exposure, the ingestion of contaminated
food or water and the inhalation of cigarette smoke. Cd causes toxicity to many vital organs including
the lungs, liver and kidneys. Studies on non-occupationally exposed individuals have demonstrated
that renal tubule dysfunction occurs at Cd concentrations as low as 50 µg/g wet weight, suggesting
that the threshold for the general population is much lower than originally thought. In fact, it is
thought that up to 1% of the general population may have significant Cd-induced kidney alterations
due to chronic exposure with low kidney Cd levels. The primary target of Cd-induced nephrotoxicity
is the S1-segment of the PT because it is the first opportunistic site of reabsorption following filtration
from the glomerulus. PT cells of the S1-segment possess a variety of transporters, metabolising
enzymes and receptors, which are essential for Cd uptake into the cell. Cd-induced cell death of PT
cells in vivo causes a general transport defect that mimics the de Toni-Debré-Fanconi-Syndrome. The
type of cell death induced by Cd differs, depending on the concentration, exposure time and cell type.
Generally speaking, acute exposure to high concentrations of Cd leads to necrosis, whereas following
exposure to low Cd concentrations, apoptotic cell death predominates. Similar effects are seen both in
vitro and in vivo. Apoptotic cell death induced by chronic intoxication with low concentrations of Cd
or Cd-metallothionein in vivo can be mimicked in a cell culture model, the WKPT-0293 Cl.2
immortalized cells derived from the S1-segment of rat kidney PT. Cd (10-50µM) induces a rapid
increase in reactive oxygen species (ROS) (≥ 30min) without any apparent mitochondrial dysfunction.
The sphingolipid ceramide has been identified as an important second messenger in apoptosis. Short
exposure to Cd (3 hours) causes an increase in ceramides, which occurs downstream of ROS
formation, that may interact with cellular components, such as endoplasmic reticulum and
mitochondria. Following apoptosis initiation, execution must take place. The classical executioners of
apoptosis are caspases, a family of cysteine proteases. However, increasing studies report caspaseindependent apoptosis, which questions the essentiality of caspases for apoptosis implementation.
With low micromolar Cd concentrations (<10 µM), caspases are only activated after 24 hours and not
at earlier time points, which supports the notion of caspase-independent apoptotic cell death. Due to
increased cytosolic Ca under pathological conditions, a role for the Ca-dependent proteases, calpains,
has emerged. Calpain activation by Cd (3-6 hours) seems to be regulated by ceramide levels, in order
to induce apoptosis. Calpain and caspase substrates overlap but they are cleaved differently to yield
different fragments, which may explain their diverse downstream targets. Furthermore, calpains and
caspases may interact with one another to enhance, as seen by Cd, or diminish apoptosis.We conclude
that Cd-induced apoptosis of PT cells entails increase of ROS, endogenous ceramide elevation and
subsequent Ca-dependent calpain activation, which propagates kidney damage by Cd.
Funded by DFG TH 345/8-1. 10-1 and 11-1
Keywords: Kidney toxicity; Apoptosis signaling; Cadmium; Calpains; Reactive oxygen species
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Microsatellite markers of immune responses gene as a
tool for immunogenetic analysis of parasitological
disease.
Mihoko Kikuchi1 and Kenji Hirayama2
1. Center of International Collaborative Research, Nagasaki University, Nagasaki, Japan
2. Dept. Immunogenetics, Institute of Tropical Medicine, Nagasaki University.
Genomic polymorphism between individuals can arise through several different mechanisms,
which include single nucleotide changes, deletions and insertions and variable numbers of simple
sequence repeats. Microsatellites have been extensively used for DNA profiling, aiming primarily at
the determination of the number and types of repeats. The cause of length changes in microsatellite
repeats is replication slippage, caused by mismatches between DNA strands while being replicated
during meiosis. Typically, slippage in each microsatellite occurs about once per 1,000 generations.
Length changes of microsatellites within promoters and regulatory regions can also change gene
expression quickly, between generations. The human genome contains many (>16,000) microsatellites
in regulatory regions. Microsatellites within introns also influence phenotype, through means that are
not currently understood. Microsatellite on immune responses related gene polymorphisms are related
to disease susceptibility/resistant directly or indirectly and the frequencies of polymorphisms are
maintained by adaptation to the environment.
Analysis of microsatellite was carried out using PCR-based genotyping fluorescence-labeled
primers were set relative to the immune responses gene regions in human genome. PCR-based
analysis is convenience and easy to screen many samples with in relatively low cost. We have listed
about 150 to 200 immune responses genes and tested microsatellite markers on individual’s gene.
In the present study, we show two preliminary studies on 1) microsatellite analysis to detect
immune responses genes for susceptibility / resistance in patients with Schistosomal fibrosis in
Philippines, and 2) identify linked genes which can be selected by malaria pressure in Vanuatu. This
identification confers functional divergence that can be used to elucidate the underlying mechanism of
natural selection.
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SESSIONS 3
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Naturally Exposed Animal Populations as a BioBio-indicator
of Environmental Pollution by Cadmium
Wisa Supanpaiboon 1, Narissara Chantaraprathet 1, Wiphawi Hipkaeo 2 and Supaporn Chenchoojit 3
1
Department of Biochemistry, Faculty of Medical Science, Naresuan University, Phitsanulok 65000 Thailand
Department of Anatomy, Faculty of Medical Science, Naresuan University, Phitsanulok 65000Thailand
3
Department of Community Health, Faculty of Sciences, Burirum Rajabhat University, Burirum 31000
Thailand
Corresponding author: supanpaiboon@yahoo.com
2
The investigations of using natural animals living in the contamination site have been
reported to be a potential indicator of environmental contamination. Cadmium is a toxic metal of
considerable occupational and environmental concerns. Exposure to cadmium has also been linked to
renal dysfunction, cancers and various diseases. Environmental monitoring of cadmium in Mae Sot
District, Tak Province has shown the contamination throughout the community and exposure to
cadmium and health consequences among residents who currently live in has been concerned. The use
of bandicoot rats (Bandicota indica) environmentally exposed and lived in cadmium contamination
area, Mae Sot, compared to the same species of rodent living in Hauymex District, Kalasin Province
where the environmental samples (soil and rice) were assessed at low cadmium contamination
indicated a good indicator of cadmium contamination. Results showed that cadmium accumulations in
liver and kidney tissues of rats lived in contamination area were significant higher compared to rats in
control area (p < 0.05). The mean concentrations in liver were 144 and 54 and in kidney were 1,035
and 300 µg/kg detected in rats trapped in contamination and control areas, respectively. The
concentrations in liver and kidney were used to estimate the amount in the body in three different
groups based on their body weight: large (> 301 g), medium (181-300 g) and small (50-180 g).
Cadmium accumulations were found statistically higher concentrations with the increased size groups
(p < 0.05). No significant different between high and low exposure groups and iron and zinc in both
tissues was found. Results suggest the higher exposure of rats from living in contamination area and
bandicoot rat can be used as bio-indicator of cadmium contamination and exposure of the residents.
Cadmium has long half life in the body; the increased accumulation with body weight suggests that
the accumulation might be increased by age or the larger amount of food consumption.
Keywords: environmental contamination, cadmium, bioindicator, bandicota, Mae Sot, Tak
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CadmiumCadmium-induced Toxicity in Bank Voles (Bandicota
indica) from HighHigh- versus LowLow-Exposure Areas
Wiphawi Hipkaeo
Department of Anatomy, Faculty of medical Science, Naresuan University, Phitsanulok, Thailand.
Correspondence : wiphawih@nu.ac.th
Cadmium (Cd) is a common pollutant of the smelting, plating, and mining industries. It is a
heavy metal with known toxicity to liver and kidney. The aim of this study was to determine the
effects of environmentally exposed cadmium in the livers and kidneys of the bank voles (Bandicota
indica) from high- versus low-cadmium exposure areas as a bioindicator for humans who are living in
the same affected areas. The bank voles, great bandicoots, were trapped from high-cadmium exposure
areas, Mae Sot, Tak, Thailand. The control groups were trapped from low-cadmium expossure areas,
Huai Mek, Kalasin, Thailand. To confirm the cadmium exposure, the cadmium concentrations in soils
and rice grains from both studied areas were measured. The cadmiums in liver and renal tissues were
also measured. The histopathological changes in the livers and kidneys of the rats were examined. The
immunolocalization of metallothionein (MT), cysteine-rich metal binding and detoxifying protein, in
the rat livers were studied. The expressions of metallothionein 1a and 2a (MT1a & MT2a) genes in
the rat kidneys were also studied by RT-PCR. Our results demonstrated that the cadmium in livers and
renal tissues were increased according to the weight of animals and significantly higher in the rats
from high-cadmium exposure areas. Microscopically, the histopathological changes of the rat livers
with the granular inflammations, perivascular inflammation and fibrosis were observed. Furthermore,
the multilobular necroses, cytoplasmic granulation in the proximal tubular cells and renal tubular
dilatations were particularly observed in the rat kidneys from high-cadmium exposure areas. In
addition, the immunolocalizations of MT in the rat livers were demonstrated with high
immunoreactivities surrounding the portal areas. Interestingly, by RT-PCR, we have found that the
expressions of MT1a were not different in both groups, in contrast with the expression of MT2a
which tended to be decreased in the rat kidneys from high-cadmium exposure areas. These results
suggested that the cadmium-induced toxicity in bank voles (Bandicota indica) from high-cadmium
exposure areas and were useful to indicate the health of the people living in the same areas.
Keywords : admium; Histopathology; Immunohistochemistry; Metallothionein
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Essential Metals and Cadmium Toxicity in the
the Kidney
David A Vesey.
Centre for Kidney Disease Research (CKDR), The University of Queensland, Princess Alexandra
Hospital, Brisbane, Queensland 4102, Australia.
David_Vesey@health.qld.gov.au
Cadmium is a toxic metal with a propensity to accumulate in the proximal tubules cells of the kidney.
This can cause tubular dysfunction with development of a renal disease resembling Fanconi
Syndrome, (failure to reabsorb electrolytes and nutrients), which may eventually progress to renal
failure. Although the clinical affects of cadmium in the kidney have been well described there is still
uncertainty about how the metal is transported and taken up by cells. As cadmium is a non-essential
metal it is unlikely that specific transport proteins exist. Rather by a process termed “molecular
mimicry” transport and storage proteins for essential metals such as iron, zinc and calcium are thought
to be responsible. Studies have shown that when dietary essential metals are in short supply, and
deficiencies develop, the expression of certain intestinal metal transporters are raised with an apparent
increase in cadmium induced toxicity. Zinc influx transporters (such as ZIP8, 10 & 14) are implicated
in cadmium uptake by cultured cells while zinc efflux transporters, notably ZnT-1, may provide
resistance to cadmium accumulation. The Divalent Metal Transporter 1, (DMT1), has been shown to
be important in cadmium absorption from the small intestine. Metallothioneins (MT) are inducible
high-affinity metal-binding proteins which transport and sequester intracellular cadmium and prevent
its toxicity. A greater understanding of the transport and cellular uptake mechanisms for essential
metals and cadmium may result in better strategies to limit cadmium accumulation and its subsequent
toxicity.
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SESSIONS 4
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Maternal and earlyearly-life cadmium exposure in rural
Bangladesh
Maria Kippler and Marie Vahter.
Institute of Environmental Medicine, Karolinska Institutet, Stockholm, Sweden.
Cadmium is a widely distributed environmental pollutant. Long-term, low-dose exposure has
been associated with impaired kidney function, which is the basis for the current risk assessment.
However, recent studies indicate that the risk for osteoporosis and hormone-related cancers is
increased at similarly low exposure levels. Also, very little is known about effects of early-life
exposure. The main sources of exposure to cadmium are our most important food products, such as
cereals, vegetables, and certain seafood. UNEP has recently emphasized the need to improve exposure
assessment for cadmium in developing countries.
Our ongoing research, involving a large, longitudinal mother-child cohort in rural Bangladesh, aims at
assessing the short- and long-term health effects of early-life exposure to toxic substances, such as
arsenic and cadmium. The study is nested into a large, randomized, population-based food and
micronutrient supplementation trail in pregnancy (MINIMat) in Matlab, 53 Km south-east of Dhaka.
We assessed maternal and early life exposure to cadmium (N=900) and interactions with nutrition. In
this area, the main staple food is rice, known to easily take up cadmium from soil. Malnourishment is
frequent and about one third of the women (14-44 years, all non-smokers) had BMI <18.5. The birth
weight is about 2,700 g, with 30% below <2,500 g. Maternal cadmium exposure was assessed by
concentrations in maternal urine, blood (erythrocyte fraction) and placenta, while early-life exposure
was assessed by cadmium in cord blood, breast milk and child urine. We used inductively coupled
plasma mass spectrophotometry (ICPMS), after microwave-assisted high temperature acid digestion.
Cadmium concentrations in maternal erythrocytes and urine were clearly elevated (median values 1.1
and 0.59 µg/L, respectively) and close to levels which are known to increase the risk of adverse health
effects. Probably, the main source of cadmium is rice. Women with low iron stores had higher
cadmium concentrations, indicating increased intestinal uptake via e.g. the divalent metal transporter
1 (DMT1), which is up-regulated at low iron stores. Interestingly, this increased cadmium uptake
occurred mainly in women with adequate zinc status, probably because zinc is essential for DMT1
regulation. We found no evidence of cadmium uptake via zinc transporters. Concentrations in cord
blood were low, but increased with increasing maternal exposure. Cadmium accumulation in placenta
was associated with lower zinc transfer to fetus, probably also lower birth weight. Cadmium transfer
to breast milk was low, but seemed to be mediated via the active transport systems utilized by iron
and manganese. In addition, cadmium appeared to impair calcium transport in the mammary gland,
possibly by blocking calcium transporters.
References
Kippler et al. Influence of iron and zinc status on cadmium accumulation in Bangladeshi women.
Toxicol Appl Pharmacol. 222, 221-226, 2007.
Kippler et al. Cadmium interacts with the transport of essential micronutrients in the mammary gland.
Toxicology. 257, 64-69, 2009.
Kippler et al. Factors influencing intestinal cadmium uptake in pregnant Bangladeshi women - A
prospective cohort study. Environ Res.109, 914-21, 2009.
Kippler et al. Accumulation of cadmium in human placenta interacts with transport of
essential elements to the fetus. Toxicol Lett. [Epub Oct 22, 2009]
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Cadmium and AgeAge-related Macular Degeneration
Nilesh M. Kalariya1, Nancy K. Wills1, Kota V. Ramana2, Satish K. Srivastava2, Sadagopa VM Ramanujam3,
Frederik J. van Kuijk1.
1Department of Ophthalmology & Visual Sciences, University of Texas Medical Branch, Galveston, TX 77555, USA.
2Department of Neuroscience, Department of Biochemistry and Molecular Biology, University of Texas Medical Branch,
Galveston, TX 77555, USA.
3PMCH-Human Nutrition, University of Texas Medical Branch, Galveston, TX 77555, USA.
Correspondence authors: fjvankui@utmb.edu; nkwills@utmb.edu
Purpose: Tobacco smoking and aging are among the few factors linked to age-related macular
degeneration (AMD), a major cause of blindness in the elderly. Recent studies indicate that cadmium (Cd) is
higher in the retinas of smokers compared to non-smokers which indicate a plausible role for Cd in the
development of AMD. We determined the effects of age and gender on Cd accumulation in human retinal
tissues such as neural retina, retinal pigment epithelium (RPE), and choroid. Since Cd, zinc(Zn) and copper(Cu)
bind to similar proteins, we hypothesized that Cu and Zn contents of human retinal tissues change as functions
of Cd accumulation during aging. Hence, we assessed the distribution of Zn and Cu in the neural retina, RPE
and choroid in male and female donor eyes. We also determined Cd levels in human retinal tissues from eyes
afflicted with AMD compared to non-diseased eyes (controls) from age-matched donors. Methods: Human
donor eyes were assessed for AMD severity using color stereoscopic fundus photographs and the Minnesota
Grading System. Cd levels in cultured RPE cells or retinal tissues isolated from donor eyes were measured using
inductively coupled plasma mass spectrometry (ICP-MS) and graphite furnace atomic absorption
spectrophotometry (GF-AAS). Toxic effects of Cd in ARPE-19 cells were determined using cell viability and
apoptotic assays. Cd induced MAPK signaling pathways in ARPE-19 cells were also determined using western
blot. Results: Our results indicate higher Cd levels in all retinal tissues from aged eyes (> or = 55 yrs) compared
to young eyes (< 55 yrs). There were significantly higher Cd levels in neural retina and RPE in older females
compared to age-matched males indicating existing gender differences in terms of Cd accumulation in retinal
tissues. Moreover, higher Cd levels were found in the neural retina and RPE of eyes afflicted with AMD
compared to non-AMD. In choroidal tissues, mean Cu and Zn levels were higher in aged donors (> or =55 yrs)
than young donors (<55 yrs) whereas in the neural retina, Cu and Zn both significantly decreased as a function
of age. Several sex-related differences were found in the RPE such as Cu levels were significantly higher in
males than in females. In addition, both Zn and Cu levels in males were positively correlated with Cd content,
whereas this association did not occur in females. Toxic effects of Cd were observed in in vitro ARPE-19 cell
culture model. Cd-exposed ARPE-19 cells showed altered cell morphology, decreased cell survival, increased
ROS levels, disruption of membrane integrity, altered mitochondrial membrane potential, cytochrome-c release,
and apoptotic changes. Depletion of intracellular GSH by buthionine-[S,R]-sulfoximine (BSO) resulted in
increased Cd toxicity in ARPE-19 cells. Cd also caused activation of mitogen-activated protein kinases
(MAPKs) pathway including c-Jun N-terminal kinase (JNK), extracellular signal-regulated kinase 1/2 (Erk1/2),
and p38 in ARPE-19 cells. Antioxidants such as N-acetylcysteine (NAC) significantly reduced Cd-induced
toxicity. Conclusions: Our results from normal human retinas indicate that cadmium accumulates differentially
in the neural retina and RPE of older men and women. Furthermore, Cd accumulation in retina was associated
with the presence of AMD at least in males. These finding raise the possibility that Cd could disrupt the
metabolism of other metals (such as Zn, Cu, etc.) in the human retina. The results are consistent with coregulation of Zn and Cu stores in retinal tissues and suggest that the balance of these metals is associated with
Cd accumulation and gender. Moreover, Cd-induced elevated ROS could activate MAPK signaling pathway
leading to RPE cell apoptosis which could lead to AMD and other retinal diseases particularly related to
smoking.
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SESSIONS 5
Cadmium conference 2010
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Environmental
Environmental cadmium exposure and oral disease
Manish Arora1,2, Jennifer Weuve1,3, Joel Schwartz1,4, Robert O. Wright1,4
1
Environmental and Occupational Medicine and Epidemiology, Harvard School of Public Health, 677
Huntington Avenue, Boston 02115, Massachusetts, USA
2
Population Oral Health, Faculty of Dentistry, University of Sydney, 1 Mons Road, Westmead 2145,
New South Wales, Australia
3
Rush Institute for Healthy Aging, Rush University Medical Center, 1653 W. Congress Parkway,
Chicago 60612, Illinois, USA
4
Channing Laboratory, Department of Medicine, Brigham and Women’s Hospital, Harvard Medical
School, 181 Longwood Avenue, Boston 02115, Massachusetts, USA
Correspondence author: marora@hsph.harvard.edu
Cadmium (Cd) is a ubiquitous toxicant in our environment, and an estimated 2.3% of the U.S.
population has elevated levels of urine Cd (>2 µg/g creatinine), a marker of chronic exposure and
body burden. We present data from three studies that explored the relationship between environmental
Cd exposure and common oral diseases. In adults (>18 years old) we examined the association of
urinary Cd concentrations with periodontal disease (a common inflammatory disease of tissues that
support teeth) and tooth loss, using cross-sectional data from the third National Health and Nutrition
Examination Survey (NHANES III). In children we undertook two studies; firstly, we examined data
from the NHANES III to explore the association of urinary Cd concentrations with dental caries
(measured as the sum of decayed and filled tooth surfaces). Secondly, to understand the biological
mechanisms behind the Cd-dental caries link, we undertook a pilot study in children living near a
mining site in Oklahoma, USA, and examined the association of saliva-cadmium concentrations with
alterations in salivary gland function, which, according to our hypothesis, may be one mechanism by
which cadmium increases the risk of dental caries. In children, an interquartile range (IQR) increase in
creatinine-corrected Cd concentrations (0.21 µg/g creatinine) corresponded to a 30% increase in the
odds of having experienced caries in deciduous teeth (prevalence OR = 1.30; 95% CI, 1.01–1.67).
Data from our pilot study in children showed that 1 ng/mL increment in saliva Cd was associated with
a 5% decrease in total protein concentrations (p<0.038), after adjusting for age, gender and
environmental tobacco smoke. Reduction in saliva protein indicates disruption of salivary gland
function. In adults, the age-adjusted geometric mean urine Cd concentration (µg/g creatinine) was
significantly higher among participants with periodontal disease [0.50; 95% confidence interval (CI),
0.45–0.56] than among those without periodontal disease (0.30; 95% CI, 0.28–0.31). Multivariableadjusted analyses, which included extensive adjustments for tobacco exposure, showed that a 3-fold
increase in creatinine-corrected urinary Cd concentrations [corresponding to an increment from the
25th (0.18 µg/g) to the 75th (0.63 µg/g) percentile] was associated with 54% greater odds of prevalent
periodontal disease (odds ratio = 1.54; 95% CI, 1.26–1.87). Overall, the results of these crosssectional studies suggest that environmental cadmium exposure may increase the risk of common oral
diseases. Further animal experiments and prospective epidemiologic research are needed to confirm
these findings and identify the biological mechanisms behind the association between environmental
cadmium exposure and oral diseases.
Keywords: Cadmium; Dental caries; Periodontal disease; Saliva; Tooth loss
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Cadmium carcinogenesis: Lessons from renal toxicity
studies
Frank Thévenod1, Prabir K. Chakraborty1, Wing-Kee Lee1, Ulrich Bork1, Natascha A. Wolff1, Blazej
Torchalski1, Malte Molitor1, Anna Kuchler1 and Naschla Kohistani1
1
Department of Physiology and Pathophysiology, University of Witten/Herdecke, Stockumer Str. 12,
D-58453 Witten, Germany
Correspondence author: frank.thevenod@uni-wh.de
Cadmium (Cd) damages the kidney by apoptosis, but exposing kidney proximal tubule cells
(PTC) to low micromolar concentrations of Cd induces the expression of cell proliferation and
survival genes. These protective mechanisms may be of importance because chronic Cd exposure has
been found associated with epithelial cancers (e.g. lung, liver, prostate, pancreas, kidneys). Therefore
Cd has been classified as a class-1 carcinogen. The present consensus is that a Cd is a weak direct
mutagen but promotes carcinogenesis induced by mutagens if combined with other pro-carcinogenic
effects of Cd, such as formation of reactive oxygen species (ROS) and/or interference with antioxidative enzymes, inhibition of DNA repair enzymes, deregulation of cell proliferation, interference
with the balance between pro and anti-apoptotic mechanisms, and disruption of cell adhesion.
Apoptosis protects cells against oncogenesis through elimination of mutant or transformed cells.
Evasion of apoptosis is a hallmark of cancer development. Thus, a better understanding of acquired
resistance to apoptosis in carcinogenesis could contribute to the development of strategies for cancer
prevention and novel cancer therapeutics. Using a culture model of rat kidney PT, the WKPT-0293
Cl.2 immortalized cells derived from its S1-segment cellular mechanisms were identified which may
contribute to Cd carcinogenesis: (i) As a multi-step process, carcinogenesis is frequently associated
with p53 inactivation. Cd is known to inactivate p53 and G2/mitosis(M) arrest contributes to
stabilization of p53-deficient mutated cells. In p53-inactivated PTC Cd-induced ROS formation and
DNA damage trigger signaling of check-point activating kinases ATM/ATR to cause G2/M arrest,
which may promote survival of pre-malignant PTC and carcinogenesis. (ii) Previously we showed Cd
apoptosis is mediated by ceramide (Cer)-calpain signaling, but Cd also upregulated multidrug
resistance P-glycoprotein (MDR1/Abcb1) to promote PTC survival. Rather than exporting Cd, we
show that Abcb1 protects against cell death by reducing cellular Cer. (iii) Cd disrupts the Ecadherin/ -catenin complex of epithelial adherens junctions (AJs). -catenin has two functions: as a
latent signaling molecule of the Wnt pathway and as a structural protein in AJs, by bridging Ecadherin to -catenin. In Wnt signaling, β-catenin is a co-activator of the LEF/TCF transcription
factor to activate cell proliferation and survival genes. Thus -catenin can be seen as a tumor
promoter and E-cadherin as a tumor suppressor. We investigated Wnt signaling after Cd-induced Ecadherin disruption in PTC. Cd triggered a Wnt response involving upregulation of proliferation
genes c-Myc and cyclin-D1, and of survival gene Abcb1. Wnt signaling elicited by Cd was more
prominent in proliferating subconfluent than confluent cells, which showed increased E-cadherin
expression. E-cadherin overepression reduced Wnt signaling, PTC proliferation and Cd toxicity.
Hence Cd may facilitate PTC carcinogenesis by inducing Wnt signaling to promote proliferation and
survival of pre-neoplastic cells. Furthermore, exposure of mice to Cd (100mg/l in tap water) for 12
weeks induced the expression of Wnt pathway components in vivo and also triggered epithelial-tomesenchymal transition which is a prerequisite for renal fibrosis and cancer. These processes may
jointly or independently promote Cd carcinogenesis in the kidney and other organs.
Funded by DFG TH 345/8-1. 10-1 and 11-1
Keywords: Renal cell carcinoma; Wnt signaling; Multidrug resistance P-glycoprotein; Cell cycle;
EMT markers
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MOLECULAR BIOLOGY OF NICKEL CARCINOGENESIS
J. R. Landolph, Jr , A. T. DeSilva, D. Mai, P. Samala, and J. Lin.
Depts. of Molecular Microbiology/Immunology and Pathology, USC Cancer Center, Keck School of
Medicine, Univ. Southern California, Los Angeles, Calif., 90033, USA..
e-mail: landoph@usc.edu
Nickel (Ni) refinery workers who inhaled Ni-containing sulfidic ore dusts and smoked
cigarettes in Ni refineries contracted lung and nasal cancers. Inhalation of Ni3S2/green NiO also
induces respiratory cancer in rats. We showed Ni3S2 and green and black nickel oxides were
phagocytosed into and induced chromosomal aberrations, cytotoxicity, and morphological, A. I., and
neoplastic transformation in C3H/10T1/2 Cl 8 mouse embryo cells. We found 130 genes were
differentially expressed between non-transformed and two 3-methylcholanthrene (MCA)-/four Nitransformed 10T1/2 cell lines by mRNA differential display. Ni/MCA-transformed cell lines
displayed a) ect-2 gene amplification/higher levels of ect-2 gene mRNA/protein; higher levels of b)
calnexin mRNA/protein and c) Wdr1 gene mRNA; and d) decreased levels of DRIP/ TRA80, and β-2centaurin mRNAs.
We hypothesized Ni+2 -induced 1) amplification of ect-2 gene/higher levels of rhoA-GTP led
to higher levels of microtubules (MTs), and 2) silencing of β-2-centaurin gene, caused higher
levels/aggregation of microfilaments (MFs), and 3) silencing of the DRIP/TRAP80 gene caused
aberrations in Ca+2 ion gradients, in transformed 10T1/2 cells. To test these hypotheses, we stained
cells with fluorescent phalloidin to decorate MFs, separately with fluorescent antibody to α-tubulin/βtubulin to decorate MTs, then separately with Fluo 3AM to stain Ca+2 ions, then examined cells by
confocal microscopy. In non-transformed 10T1/2 cells, MFs/MTs were arranged homogeneously in
long thin fibers. In NiS/green NiO transformed cell lines, MFs and MTs were over-expressed and
aggregated in some areas, absent in other areas, changing shapes of transformed cells, rounding
them/altering their contact with extra-cellular matrix. In non-transformed cells, Ca+2 ions were found
in two arrangements in non-transformed 10T1/2 cells: State I, in low density cells, with a heavy
concentration of Ca+2 ions in the nucleus, and lesser amounts in the cytoplasm; and State II, in high
density cells near confluence, where there were few Ca+2 ions in the nucleus, most in the cytoplasm.
Non-transformed 10T1/2 cells cycled between States I and II. In Ni/MCA transformed cell lines, Ca+2
ions were predominantly cytoplasmic (State II). Our model suggests mutations in 15 genes led to
differential expression of 130 total genes. We conclude Ni ions caused amplification of the ect-2
gene, leading to expression of higher steady-state levels of MFs and MTs, causing changes in cell
shape, hence changes in global gene expression. Ni ions also silenced the DRIP/TRAP80 gene, which
likely led to alterations in Ca+2 ion gradients in transformed cells, further altering activities of Ca+2
ion-dependent enzymes and cellular physiology. These Ni ion-induced events cumulatively led to
differential expression of 130 genes in transformed cell lines, altered cell shapes, and altered Ca+2 ion
gradients, contributing to induction and maintenance of transformed phenotypes of transformed cell
lines. Supported by grants R01 ES0-3341/NIEHS (PI, JRL) and 5 T32 AI07078/NIAID, USC
Discretionary Funding.
Key Words: Nickel, oncogenes, suppressor genes
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SESSIONS 6
Cadmium conference 2010
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International Food Legislation
Soisungwan Satarug*,1 ,2 and Michael R. Moore1
*
Honorary Research Fellow, 1National Research Centre for Environmental Toxicology, Brisbane, Queensland,
Australia, 2Visiting Research Professor, Pathology Department, University of North Dakota School of Medicine
and Health Sciences, Grand Forks, ND 58202, USA.
Cadmium occurs naturally in the earth’s crust in relatively low abundance. Cadmium occurs in high
abundance in ores together with zinc, copper and lead. Cadmium is used as an anticorrosion agent, stabilizer in
polyvinyl chloride products, color pigment, and rechargeable Ni–Cd batteries.
Industrial application of
cadmium coupled with negligible success rates of recycling have led to a widespread dispersion of cadmium
into the general environment. Cadmium is non-biodegradable and its persistence in the environment results in
bio-accumulation. In addition, over application of phosphate fertilizers (some may contain high levels of
cadmium) results in upward trends of cadmium content agricultural soil and the produce.
In 2000, the Codex Committee for Food Additives and Contaminants (CCFAC) reached agreement on
the principles for setting maximum limits (MLs) for contaminants although the Joint FAO/WHO Codex
Alimentarius Commission was established in the early 1960s to detail international food legislation. MLs were
proposed for cadmium in various food categories, including rice, soybean, bivalve mollusks, and peanuts all of
which have been traded internationally. Bivalve mollusks and crustaceans are filter feeders that accumulate
metals from the aquatic environment independent of environmental pollution and their cadmium contents are
usually >1-2 mg/kg wet weight. Current ML for bivalve mollusks has been lowered from 2 to 1 mg/kg wet
weight. Low bioavailability (low absorption rates) of cadmium has been deployed in arguing for assigning high
cadmium ML values to allow the marketing of oysters and their products which contain naturally high levels of
cadmium. However, that there is no distinction between toxicity of natural vs. anthropogenic cadmium and
bioavailability of cadmium in oysters has now been shown.
Safe intake guidelines have been established for cadmium by the Food and Agriculture
Organization/World Health Organization (FAO/WHO) Joint Expert Committee on Food Additives (JECFA).
The Provisional Tolerable Weekly Intake (PTWI) value initially set for cadmium was 400–500 µg per person
per week (WHO, 1989). These levels were based solely on a critical renal concentration of 100-200 µg Cd/g
wet kidney cortex weight, attainable after a cadmium intake of 140–260 µg/d for over 50 yrs or 2000 mg over a
lifetime. The PTWI model incorporates an oral absorption rate of 5% and a daily excretion rate of 0.005 % of
total body burden. An extremely slow elimination rate for cadmium ensures cumulative cadmium levels in
tissues and organs over long-term consumption/exposure. In 1992, the PTWI for cadmium was refined and
subsequently expressed in terms of cadmium intake per kg body weight (WHO, 1993). This refinement also
recognized that the model PTWI for cadmium did not include a safety factor and that there was only a very
modest margin between the level of exposure in a normal diet and a level predicted to produce effects on the
kidney. Despite the narrow safety margin, the PTWI for cadmium at 7 µg/kg body weight was retained, which
is translatable to 70 µg per day for a 70-kg person. A toxicokinetic model predicts, based on similar
assumptions, that the renal cortical cadmium level of 50 µg/g wet weight could be attained at the cadmium
intake of 1 µg /kg body weight/day over 50 yrs, which is the same as the current FAO/WHO guideline. The
renal cortical cadmium 50 µg/g wet weight corresponds to urinary cadmium 2 µg/g creatinine, but kidney effects
have been observed at urinary cadmium levels as low as 1 µg/g creatinine. These findings suggest that current
intake guideline (at 70 µg per day for a 70-kg person does not provide sufficient health protection. With a
similar consideration of the kidney as a toxicity target, however, the European Food Safety Agency (2009)
lowered the cadmium the tolerable weekly intake from 7 to 2.5 µg/kg body weight, translates into 25 µg per day
for a 70-kg person. We have validated the PTWI model by studying cadmium accumulation in kidneys and
livers of environmentally exposed subjects. To account for exposure through inhalation, we measured cadmium
content in the lung together those of the kidney and liver. Cadmium accumulation in kidney cortex increased
with age, reaching a plateau by 50 yrs of age. An estimated dietary intake at 25–30 µg cadmium per day for the
41-50-y peak-age group would give rise to total cadmium body burden 18 mg. These studies predict that the
estimated intake of 25-30 µg/day may produce adverse kidney effects in about 1 % of the adult population when
variability in absorption and sensitivity to adverse effects among population members are considered in the
analysis. Our studies suggested that the safe intake cadmium level for an adult should be below 30 µg per day,
in agreement with the advice of the European Food Safety Agency.
NB: JECFA has defined the PTWI for a chemical with no intended function as an estimate of the amount of the
chemical that can be ingested weekly over a lifetime without appreciable health risk.
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NHANES Cadmium Biomonitoring Studies in the General
U.S.
1
1
Population – An Overview
B A Fowler, 1 P Ruiz, 1 M Mumtaz, 2 J Osterloh
Division of Toxicology and Environmental Medicine, ATSDR; 2Division of Laboratory
Sciences, NCEH
Cadmium occurs naturally in the environment and exposure of the general population to
cadmium is predominantly through diet. Smoking is another important source of exposure to
cadmium. Chronic exposure to cadmium is a public health concern because it is known to accumulate
and cause kidney damage. The National Health and Nutritional Examination Survey (NHANES) has
proved to be a valuable tool for assessing concentrations of a number of toxic chemicals in a
representative sample of the general U.S. population. Cadmium has been measured in three
NHANES cycles (1999-00, 2001-02, 2003-04. In the December 2009 released NHANES survey,
cycle 2003-04, urinary cadmium measurements are available on 2257 persons aged 6 year and older.
Results of these biomonitoring studies have suggested variations in cadmium exposure in the general
U.S. Population over time but that exposure variations within the population also occur as a function
of smoking and diet but also age. Recently, computational toxicology models have been developed
based on NHANES and other available cadmium data using Berkeley – Madonna software to predict
the urinary excretion of cadmium. These models replicate the NHANES data very well. Preliminary
modeling studies using this model suggested increased exposure/uptake of cadmium among persons
in the range of 8-12 years followed by a continuous monotonic rise in cadmium uptake/exposure into
the 8th decade of life. The results of these studies confirm and extend previous findings on the
cumulative nature of cadmium in humans and suggest variation in exposure /uptake over the course of
a lifetime. These data coupled with findings of renal vascular damage at lower cadmium tissue levels
indicate the need for further research into cadmium induced health effects in general populations.
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RESEARCH INTO AND MANAGEMENT OF CADMIUM IN
AUSTRALIAN AGRICULTURE
M.St.J. Warne and M.J. McLaughlin.
Centre for Environmental Contaminants Research, Division of Land and Water, Commonwealth
Scientific and Industrial Research Organisation, Adelaide, South Australia, 5052, Australia. Email:
michael.warne@csiro.au
The findings in the 1970s that cadmium (Cd) present in food could be a potential threat to
human health was viewed with considerable concern in Australia as it was/is a major exporter of high
quality, “clean and green” agricultural commodities that is important to the Australian economy.
Since then, there has been considerable research conducted on Cd in Australian agriculture. This
research revealed that unlike northern hemisphere countries, atmospheric inputs of Cd to soils in
Australia have been historically low and background concentrations of Cd in Australian soils are
generally low (<0.5 mg/kg). Localised contamination of soils and crops close to large industrial and
urban centres was also identified. It was also quickly recognised that concentrations of Cd in
agricultural soils had increased through fertiliser use since the late 19th century when superphosphate
was first introduced to Australia.
Budgets for Cd in agriculture showed that the main pathway by which Cd enters Australian
agroecosystems is mineral fertilisers. Other anthropogenic sources of Cd include biosolids and to a
lesser extent composts and other soil additives. That the main source of Cd is mineral fertilizers is
significant as Australian agricultural soils are generally nutrient deficient, and thus Australian
agriculture relies on extensive fertiliser use.
To address the potential problem of increasing Cd concentrations in Australian agricultural
soils and produce, a National Cadmium Minimisation Strategy (NCMS) was established in 1999. It
was realized that only controlling the input of Cd would not be sufficient to control Cd in the food
chain and therefore the NCMS used an integrated approach of education, regulation, product
modification and research to manage Cd. In 2000, a National Cadmium Management Committee
(NCMC) was established to manage and implement the NCMS. At the end of 2006, the NCMC was
wound up as all the objectives of the strategy had been achieved. Achievements of the NCMC include
facilitating the establishment of an inter-laboratory quality assurance and accreditation program for
Cd analysis in soils and plants, development of a database for Cd concentrations in Australian
agricultural produce, a mass balance for Cd in Australia, a web-site and the publication of six best
management practice brochures for various agricultural industries. In addition, several research
projects arose from the activities of the NCMC. These included the Australian National Biosolids
Research Program that developed soil-specific limits for Cd, copper and zinc in biosolids, a project to
develop new urban soil quality guidelines for contaminants including Cd and a project that assessed
the hazard posed by contaminants in mineral fertilizers and industrial residues applied to agricultural
soil and developed guidelines for a range of contaminants in these products.
Cadmium conference 2010
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SESSIONS 7
Cadmium conference 2010
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Bioremediation
Bioremediation of cadmium contaminated irrigation and
drinking water:
A large scale approach
J.M.R.S.Bandara1,2, H.V.P.Wijewardena2 and H.M.M.S. Seneviratne2.
1 Department of Agric. Biology, University of Peradeniya, Peradeniya, Sri Lanka.
2 Board of Study in Plant Protection, Postgraduate Institute of Agriculture, University of Peradeniya,
Peradeniya, Sri Lanka
Correspondence Author: bandara.sarath@gmail.com
A comprehensive study on the “Hyper-accumulators” of heavy metals could help in designing
strategies to alleviate heavy metal problems in agricultural land and irrigation and potable water. The
existence of plant species that possess the ability to accumulate very high levels of heavy metals
without apparent phytotoxicity is an indicator of high genetic potential of plant that can clean
contaminated soil and water. Cadmium is one of the most troublesome toxic heavy metal that
accumulates in the water reservoirs and agricultural soil as a result of intensive use of Cd
contaminated phosphate fertilizers in agriculture in the North Central Province of Sri Lanka. There are
only two cadmium hyper-accumulators identified up to now. The best characterized is Thlaspi
caerulescensl, a member of the Brassicaceae family, which can accumulate up to 1000 ppm Cd in
shoots without exhibiting toxicity symptoms. A foliar Cd level above 1 ppm usually is considered
phyto-toxic. We observed that the plant species traditionally grown in water reservoirs and on either
sides of water distribution canals in NCP are excellent phyto -remediating plants. The storage
rhizomes of year old Nelumbo nucifera grown in water reservoirs accumulated 252.82+ 12.49 mg
Cd/kg. The other metals accumulated in higher levels in N. nucifera rhizomes are Cu,Co, Fe,Mn,Pb
and Zn. In a control environment study using seedlings of N. nucifera grown in 5% Hoagland’ s
solution at 0.75, 12.0 and 1.25 ppm cadmium sulphate showed a significant increase in Cd removal
0.0334 to 0.121 ppm/week was observed. However a removal rate from water remained stagnant at
higher concentrations of Cd in water. The apparent slow growth rate of plants and low rate of
phytoextraction demands a more effective but a cheaper and quicker method of remediation in order
to combat the prevailing elevated cadmium levels in NCP that causes CRF. We have developed a
large scale filtering device with the use of rice husk which is an abundant residue in rice industry. We
have achieved successful results of sequestering Cd using raw rice husk as well as amorphous silica
derived from rice husk. Presently we are studying the use of algae/lactobacillus spp. Integrated rice
husk filter as a floating device to be left in reservoirs and canals to sequester cadmium from
contaminated water that can be periodically rejuvenated to improve biological activity. The efficacy
and the mode of action of the filtering device we developed to sequester cadmium from irrigation
and potable water will be discussed.
Key words: Cadmium filter, amorphous silica, rice husk,
Cadmium conference
conference 2010
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A Study of cadmium in soils
and Vietnamese standard of cadmium in agricultural
soils
Pham Quang Ha1 and Ha Manh Thang1
1
Institute for Agricultural Environment (IAE/VAAS)
Phu Do, Tu Liem, Hanoi, Vietnam
Correspondence author: pqha-nisf@hn.vnn.vn
This paper reported the results of soil cadmium study in term of total concentration in
Fluvisols, Acrisols and Ferralsols and in some other soils in traditional rural handicraft production
villages or in peri-urbain areas. The results showed that: The average content of Cd is less than 0.5;
0.8 mg Cd/kg soil respectively for Acrisols and for Fluvisols. Meanwhile the Cd content in Ferrasols
are reached of 1 mg Cd/kg soils; it is relatively high and we should pay attention to protect this soil
for prevent Cd contamination by agricultural or industrial activity.
The study of Cd content in the traditional rural handicraft area as well as in sub peri-urban areas
warned an accumulation of Cd in mud and in sludge. The very high Cd content were observed in such
materials and it is an alarm to protect this area and preventing using river or lake city mud for
planting food crops such as vegetables for examples.
Vietnamese standard of heavy metals such as Cu, Cd, Cu and Zn in some great soil groups were
formulated and revised recently to guide cropping and inform the acceptable heavy metals in soil.
Keywords: cadmium; Vietnam soils; standard
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ORAL PRESENTATIONS
Cadmium conference 2010
40
DMSA alleviates oxidative stress and vascular dysfunction
in mice with longlong-term exposure to cadmium
Kwanjit Sompamit1, Wanida Donpunha2, Patchareewan, Pannangpetch3, Veerapol Kukongviriyapan3
and Upa Kukongviriyapan2
1
Faculty of Medicine, Mahasarakham University, Mahasarakham, 44000, Thailand
Department of Physiology, Faculty of Medicine, Khon Kaen University, Khon Kaen, 40002, Thailand
3
Department of Pharmacology, Faculty of Medicine, Khon Kaen University, Khon Kaen, 40002,
Thailand
2
Correspondence author: upa_ku@kku.ac.th
Cadmium (Cd) is the 48th element and a member of group 12 in the Periodic table of elements. The
most dangerous characteristic of Cd is that it accumulates throughout a lifetime mostly in the liver and
kidney and has a long biological half-life of 17 to 30 years in human. Several lines of evidence
indicate that reactive oxygen and nitrogen species are involved in Cd-mediated tissue damage. Meso2,3-dimercaptosuccinic acid (DMSA) is a sulfhydryl-containing, water-soluble, non-toxic, and orallyadministered metal chelator. DMSA has been found to be effective in terms of survival and lowering
the Cd contents of liver and kidney in Cd-exposure. Although the chelating properties of DMSA are
well documented, its potential to serve as an antioxidant and vascular protection in vivo had not
previously been explored. Therefore, this study was aimed to investigate the effect of DMSA against
Cd-induced oxidative stress and vascular dysfunction in mice. Male ICR mice were received Cd as
CdCl2 (100 mg/L) via their drinking water for 8 weeks. Mice received tap water were served as
normal controls. After 8 weeks, CdCl2-treated mice were randomly divided into 3 groups (n=
8/group). Mice treated with CdCl2 in group 1 and 2 were intragastrically administered with DMSA at
doses of 25 or 50 mg/kg for 5 days, respectively. Mice in group 3, served as Cd-treated controls, were
intragastrically administered with vehicle (deionized water) for 5 days. At the end of the study, mice
were anaesthetized with ketamine/xylazine (100:2.5 mg/kg, i.p.). Blood pressure, vascular reactivity,
and oxidative stress markers were determined in every groups of the study. It was demonstrated that
Cd induced hypertension and markedly blunted vascular responses to vasoactive agents. Treatment
with DMSA significantly restored blood pressure and improved vascular responsiveness when
compared with Cd-treated controls. Moreover, DMSA dose-dependently protects against Cd-induced
oxidative stress by enhancing the redox ratio of glutathione to glutathione disulfide and decreasing
plasma malondialdehyde, plasma protein carbonyl, urinary nitrate/nitrite, and superoxide production
in thoracic aortas of mice exposed to Cd. With regard to the metal chelating activity, DMSA
apparently reduced Cd concentrations in the blood, liver and kidney of mice after exposure to Cd.
This study provides the evidence on the beneficial effect of DMSA against oxidative stress and
vascular dysfunction in a mice model of Cd poisoning.
Keywords: Cadmium; DMSA; Vascular dysfunction; Oxidative stress
Cadmium conference 2010
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POSTER PRESENTATIONS
Cadmium conference 2010
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NEMO and G6PD mRNAs Expression are Reduced by
Cadmium
Cadmium in Human Hepatocellular Liver Carcinoma Cell
Line (HepG2)
Chatkul Techakitiroj 1, Wisit Tangkeangsinsin2 and Palarp Sinhaseni3
1
Department of Biochemistry and Microbiology, Faculty of Pharmaceutical Sciences, Chulalongkorn
University, Bangkok, Thailand
2
Department of Biopharmacy, Faculty of Pharmacy, Silpakorn University, Nakhon Pathom, Thailand
3
Department of Pharmacology and Physiology, Faculty of Pharmaceutical Sciences, Chulalongkorn
University, Bangkok, Thailand
Correspondence author: tverakit@gmail.com
Recently, environmental pollution by cadmium has been discovered in Mae Sot District, Tak
Province, Northwestern Thailand (Prozialeck et al., 2006). Cappellini et al. reported that about 1011.9 % of Thai people had deficient G6PD activity. The human G-6-PD gene maps to Xq28 of
chromosome X and is arranged head to head with the NF-kappaB essential modulator (NEMO, IKKγ)
gene (Galgóczy et al., 2001). In this study we investigated the effects of cadmium to NEMO and
G6PD mRNAs expression in human hepatocellular liver carcinoma cell line (HepG2). We detected
protein expression by western blot and mRNA expression by RT-PCR techniques. We found that
cadmium can decrease the expression of NEMO and G6PD mRNAs but cadmium can increase
cleavage-Poly (ADP-ribose) polymerase protein ~50 KDa depends on dose of cadmium. This is the
first report on the effect of cadmium on NEMO and G6PD genes expression in the HepG2 cells.
Keywords: Cadmium; NEMO, IKKγ, G6PD, HepG2
Cadmium conference 2010
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AntiAnti-oxidant activities of Thunbergia laurifolia Linn.
against leadlead-mediated neurotoxicity.
Jitbanjong Tangpong1*, Suksan Changlek1, Phunnee Pidetcha2, Alan F. Geater3, Soisungwan
Satarug4
1
School of Allied Health Sciences and Public Health, Walailak University, Nakhon-Si-Thammarat,
80160, Thailand
2
Faculty of Medical Technology, Mahidol University, Bangkok, 10170, Thailand
3
Epidemology Unit, Faculty of Medicine, Prince of Songkla University, Songkhla, 90112, Thailand
4
Department of Pathology, University of North Dakota School of Medicine and Health Sciences,
Grand Forks, ND, USA.
Correspondence author:rjitbanj@wu.ac.th
Lead is a heavy metal known to cause injury to a number of tissues and organs such as liver, kidney
and brain, resulting in hepatotoxicity, nephrotoxcity and neurodegenerative disease. As a neurotoxin,
lead particularly affects the developing central nervous system (CNS) and it may potentially induce
oxidative stress. In the present study, we evaluated the ability of Thunbergia laurifolia Linn. (TL)
extract to protect against neurotoxicity induced by lead treatment. Groups of mice were treated with
lead alone at the dose levels of 0.5 and 1 g/L in drinking water, lead plus TL extract, or lead plus
vitamin E. We used the Morris water maze swimming test to evaluate neuronal effects of those
treatments. In addition, we measured the activities of antioxidant enzymes, including, glutathione
peroxidase (GSH-Px) and superoxide dismutase (SOD), lipid peroxidation and protein oxidation,
caspase-3 activity in samples of plasma and brain tissues of mice. The results show that lead
treatment significantly increased GSH-Px activity while it decreased SOD activity (p<0.05). Levels
of malondialdehyde (MDA), protein carbonyl, lipid peroxidation and protein oxidation markers all
were significantly increased in lead treated mice (p<0.05). Further, elevated cell death and memory
loss were also observed probably as the result of enhanced oxidative stress and accelerated caspase-3
activity and latency time. Protective effects of treatment with TL extract and vitamin E against leadinduced neurotoxicity was evidenced from a significant increase in SOD activity in conjunction with
reduction in GSH-Px, lipid peroxidation and protein oxidation.
Conclusion: TL extract and vitamin E are shown to have the potential to protect against oxidative
stress and cell death in brain tissues, caused by lead exposure. Development of TL products may
prove be beneficial for those at high-risk of exposure to lead.
Keywords: Lead, Thunbergia laurifolia Linn. (TL), Neurotoxicity, Anti-oxidant
Cadmium conference 2010
44
Effects of aging and cadmium exposure on genomic
DNA methylation state of testes of the bandicoot
bandicoot rat
(Bandicota indica)
Narissara Chantaraprathet 1, Wiphawi Hipkaeo 2, Supaporn Chenchoojit 3 and Wisa Supanpaiboon 1
1
Department of Biochemistry, Faculty of Medical Science, Naresuan University, Phitsanulok 65000
Thailand
2
Department of Anatomy, Faculty of Medical Science, Naresuan University, Phitsanulok
65000Thailand
3
Department of Community Health, Faculty of Sciences, Burirum Rajabhat University, Burirum
31000 Thailand
Corresponding author: supanpaiboon@yahoo.com
Cadmium is a toxic metal that has been categorized as a human carcinogen. Environmental
contamination of cadmium causes the food-chain transfer and bioaccumulation. The use of natural
population of animals in biomonitoring may provide information useful for an estimate of the risk to
human health from anthropogenic source of pollution. Regulation of DNA modification is critical for
genomic stability and function. This study aimed to investigate changes in the genomic DNA
methylation state in testes of bandicoot rats, living in two geographic locations. One was in cadmium
contamination area, Mae Sot District, Tak Province. The other was in Huai Mek District, Kalasin
Province with no apparent contamination by cadmium and thus was considered to be representative of
a control, low-exposure area. Rats were divided in to three groups based on their body weight: large
(> 301 g), medium (181-300 g) and small (50-180 g). Liver, kidney and testes samples were obtained
from 45 rats from a contaminated area and from 33 rats from a control area.
Cadmium
concentrations in liver and kidney tissues were determined with a graphite furnace atomic absorption
spectrophotometer. Liver and kidney cadmium contents were used to estimate body burden of
cadmium. Metallothionein protein levels in testicular tissues of large- and medium-size groups were
analysed with immunohistochemistry. For global DNA methylation assay, genomic DNA was
isolated from samples of testes and was subjected to enzymatic hydrolysis, followed by sequential
digestion. The content of 5-methyl-2‘-deoxycytidine in the resultant digest was determined by
reversed-phase HPLC. Genomic DNA methylation state was expressed as a percentage of 5-methyl2‘-deoxycytidine in the total deoxycytidine residues. Comparison of cadmium body burden among
groups of rats has revealed that rats from a contaminated area had higher cadmium body burden than
those from a control low-exposure area (p < 0.05, Mann-Whitney Test). From both contaminated and
control areas rats with the higher body weight had grater cadmium body burden than those with lower
body weight (p < 0.05). Elevated expression of metallothionein protein was found in testis of rats
from contaminated area. However, average genomic DNA methylation of combined large- and
medium-size groups was 3.75% for those from contaminated area and it was 3.72% for those from a
control area. A positive correlation between body burden of cadmium and percent DNA methylation
was also found for the two groups. In addition, greater strength of correlation (r = 0.9870) was found
among rats of large-size groups, thereby suggesting higher DNA methylation state in older rats. It is
thus concluded that DNA hypermethylation state in the testis was influenced by both age and
cadmium exposure levels.
Keywords: DNA methylation, environmental contamination, cadmium, bioindicator, bandicota, Mae
Sot, Tak
Cadmium conference 2010
45
Histopathological Changes in the Kidney of Bank Voles
environmentally Exposed to Cadmium in the Cadmium
Contaminated Area,
Mae Sot, Tak, Thailand
Ketsarin Siriked, Supaporn Chuenchoojit, Tewarat Kumchantuek, Phongpitak Putiwat,
Kannika Phanmatchaya, Kitsaphon Kanamnouy and Wiphawi Hipkaeo
Department of Anatomy, Faculty of medical Science, Naresuan University, Phitsanulok, Thailand
Correspondence author: wiphawih@nu.ac.th
Experimentally, cadmium is a heavy metal with known toxicity to kidney. The aim of this study was
to determine the effects of environmentally exposed cadmium in the kidneys of the bank voles living
in cadmium contaminated areas as a bioindicator for humans who are living in the same affected area,
Tak, Thailand. The bank voles, great bandicoots, were trapped. The control groups were trapped from
noncadmium contaminated areas. The cadmium concentrations in both studied areas were measured.
The histopathological changes of the rat kidneys were examined. Microscopically, the
histopathological changes of the rat kidney were found especially in the necroses, cytoplasmic
granulation and tubular dilatation. These results suggested that environmental exposure to cadmium
causes kidney damage in bank voles and it might be useful to indicate the health of the people living
in these areas.
Keywords : Cadmium, Kidney, Histopathology, Bank voles, Tak
Cadmium conference 2010
46
Protective effect of ascorbic acid on cadmiumcadmium-induced
vascular dysfunction in mice
Wanida Donpunha1, Poungrat Pakdeechote1, Veerapol Kukongviriyapan2, Kwanjit
Sompamit3 and Upa Kukongviriyapan1
1
Department of Physiology, Faculty of Medicine, Khon Kaen University, Khon Kaen, 40002, Thailand
Department of Pharmacology, Faculty of Medicine, Khon Kaen University, Khon Kaen, 40002,
Thailand
3
Faculty of Medicine, Mahasarakham University, Mahasarakham, 44000, Thailand
2
Correspondence author: upa_ku@kku.ac.th
Cadmium (Cd) is one of the most important environmental and occupational metallic toxicants which
is widely dispersed in the environment. Recent studies have shown that Cd is implicated in
cardiovascular diseases such as atherosclerosis, hypertension, stroke and cardiac arrest. It has been
reported that Cd causes oxidative damage within the vascular tissues resulting in vascular
dysfunction. Numerous reports in various laboratories suggest the prophylactic effect of natural
antioxidant compounds against toxic metals. The present study was aimed to investigate whether
ascorbic acid has ability to protect against vascular dysfunction induced by CdCl2 in mice. Male IRC
mice were received CdCl2 (100 mg/L) via drinking water for two months whereas normal control
mice received deionized water. Other groups of animals treated with CdCl2 were orally administered
with antioxidant ascorbic acid at doses of 50 and 100 mg/kg/day. After the two months treatment,
mice were anesthetized with ketamine/xylazine (100:2.5 mg/kg, i.p.), arterial blood pressure was
recorded through carotid artery and vascular reactivities to phenylephrine (0.03 umol/kg),
acetylcholine (10 nmol/kg) and sodium nitroprusside (10 nmol/kg) were tested. CdCl2 administration
to mice increased arterial blood pressure and attenuated vascular responses to vasoactive agents.
These alterations were associated with increased urinary nitrate/nitrite and elevated malondialdehyde
levels in plasma and tissues. Ascorbic acid dose-dependently reduced blood pressure, improved
vascular responsiveness, decreased urinary nitrate/nitrite and suppressed lipid peroxidation. Results
of the present study suggest that supplementation with antioxidant ascorbic acid effectively protects
against CdCl2-induced hypertension and vascular dysfunction in mice.
Keywords: Cadmium; Ascorbic acid; Vascular dysfunction; Oxidative stress
Acknowledgement: This work was supported by a grant-in-aid from the Graduate School, and
Faculty of Medicine, Khon Kaen University. Wanida Donpunha was supported by Graduate
School Grant, Khon Kaen University.
Cadmium conference 2010
47
Surveillance of the FoodFood-Chain Contamination by
Cadmium in Mae Tao Mai Village
Mae Sot District, Tak Province
Winai Thongchub, Virat Prawantao,
The Office of Disease Prevention and Control 9th Phitsanulok
Cadmium enters the human body via consumption of cadmium containing food which includes food
plants of natural source, home grown plants and farm produce.
Population health effects of
consumption of such cadmium containing food are determined by both frequency and quantity of food
consumed. The present study aimed to evaluate the interrelationships between frequency and quantity
of consumption of cadmium contaminated food-chain plants and consumption behavior. Health
threatening conditions, evaluation of contact and a response estimate of effect probability were
conduced for 21 plants preferentially consumed by an affected population and were analyzed for
cadmium content. The daily consumption quantity of 25, 50, 75, and 100 gm and the weekly
consumption frequency of 3, 6, 9, and 12 were assigned into an analysis model. Of the 21 plants
analyzed, Lasia spinosa had the highest cadmium (29.19 mg/kg), followed by peak of roselle
(11.56mg/kg), edible fern (8.51mg/kg), and lemon grass (4.66 mg/kg). These cadmium levels were
higher than the Thai food standard of < 0.2 mg/kg. Hazard of food-chain plant consumption at 25
mg/day showed that Lasia spinosa, peak of roselle, and edible fern gave a hazard quotient of more
than 1 at consumption frequency of 3 times/week. Consumption rate of 25 mg/day, 12 times/week of
Lasia spinosa, peak of roselle, and edible fern give a hazard quotient of 21.27, 8.42, and 6.20,
respectively. The hazard quotient of lemon grass, elephant ear, and sesban was 3.40, 1.30, and 1.24,
respectively. The results of the present study also showed that those who consumed such plants more
frequently have a greater chance of adverse health effects despite a small quantity of consumption.
Hazard of food-chain plant consumption at 25 at a maximum of > 100 gm/day, Lasia spinosa, rosella,
edible fern, lemon grass, elephant ear, and sesban gave a hazard quotient of more than 1 at
consumption frequency of 3 times/week. Consumption rate of 100 mg/day, 12 times/week of Lasia
spinosa, rosella, edible fern, lemon grass, elephant ear, and sesban gave a hazard quotient of 85.08,
33.69, 24.80, 13.58, 5.19, and 4.95, respectively. The hazard quotients of betel, bamboo shoot, corn,
galangal, water convolvulus, sesban, peak of pumpkin tree, and banana tree were 3.70, 3.32, 3.24,
2.83, 2.33, 2.10, 1.37, and 1.05, respectively. The people with iron deficient anaemia, high blood
sugar, and underlying diseases were more profoundly affected by cadmium intoxication from
continued exposure to cadmium in high levels. The study can be of use in the development of
guidelines for prevention and control of environmentally related diseases as well as in the monitoring
of health effects together with planning for resolving the problems by relevant organizations.
Keywords: Cadmium contamination Exposure assessment Food chain plant
Cadmium conference 2010
48
Characterization of metal binding properties of CXXC motif
from Staphylococcus aureus
Sutthirat Sitthisak1, Kamala Boonyonying1, Thawatchai Kitti1 , Radheshyam Jayaswal2
and Skorn Mongkolsuk3
Department of Microbiology and Parasitology, Faculty of Medical Sciences, Naresuan University,
Phitsanulok, Thailand. 1
Microbiology Group, Department of Biological Sciences, Illinois State University, Illinois, USA2
Faculty of Sciences, Mahidol University, Bangkok, Thailand3
Correspondence author: sutthirats@nu.ac.th
The CXXC motifs are found in heavy metal chaperone, heavy metal transporter and thiol-disulphide
oxidoreductase superfamily in all living organisms. In this study, the putative MctsRa from
Staphylococcus aureus encoded a protein with 189 amino acids that contained four metal binding
domains with CxxC motif has been cloned, expressed and purified. By using IAA resin
chromatography equilibrated with different heavy metals showed the protein can bind to Cu (II), Zn,
Co (II) and Cd (II) but not Pb(II), Mg(II), Fe (III) and Mn (II). The binding was confirmed by the
ability of heavy metal to protect the cysteine residues in the metal-binding domains against labeling
with the cysteine-directed fluorescent reagent, 7- diethylamino-3-(4’-maleimidylphenyl)-4methylcoumarin (CPM). Overexpression of the MctsRa in E. coli BLR (DE3) exhibited increased
resistance to CuSO4. This indicates that these residues involved in metal binding and suggests that
they may have an important role in metal homeostasis and protein interaction.
Keyword: Metal binding, CXXC motif, Staphylococcus aureus
Cadmium conference 2010
49
Determination of trace amounts of cadmium in phosphate
fertilizer
fertilizer using a
PANPAN-Nafion® modified glassy carbon electrode
Sirirat Phaisansuthichol1,2, Roongoje Ratana-ohpas2 and Saravut Dejmanee2
1
Department of Chemistry, Faculty of Science, Maejo University, Chiang Mai, 50290, Thailand.
Department of Chemistry, School of Science, Walailak University, Nakhon Si Thammarat, 80161,
Thailand.
2
Corresponding author: dsaravut@wu.ac.th
A simple method for the determination of trace Cadmium (Cd) (II), using a disposable 1-(2pyridylazo)-2-naphthol [PAN]-Nafion® coated glassy carbon electrode, has been developed. The
modified electrode exhibited a significant improvement on both sensitivity and selectivity for Cd (II)
determination, compared with a bare glassy carbon electrode (GCE). Differential pulse anodic
stripping voltammetry was performed after the Cd (II) ion, in 0.05 M potassium hydrogen phthalate
(KHP) buffer medium, accumulated on the PAN-Nafion® surface of the glassy carbon working
electrode through the formation of a chemical complex at an open circuit. The modified GCE with Cd
(II) complex is then transferred to a 0.1 M KI solution and subjected to an electrochemical stripping
procedure. Affected parameters were optimized to yield the most suitable conditions, including the pH
and concentration of the accumulation medium, deposition potential, deposition time and amount of
coated PAN-Nafion®. The quantitative analysis of contaminated cadmium in phosphate fertilizer
samples has been carried out. The results obtained from the proposed method agree well with those
obtained by inductively coupled plasma-optical emission spectrophotometry.
Keywords: Cd (II), PAN- Nafion®, modified glassy carbon electrode, phosphate fertilizer, Stripping
voltammetry
Cadmium
Cadmium conference 2010
50
Fractionation of zinc, cadmium and lead in contaminated
soils by using
the BCR sequential extraction procedure
Kanya Kerdsiri1, Janpen Intaraprasert2 and Ponlayuth Sooksamiti3
1
Division of Chemistry, Faculty of Science, Ubon Ratchathani Rajabhat University, Ubon
Ratchathani, 34000
2
Department of Chemistry, Faculty of Science, Ubon Ratchathani University, Ubon Ratchathani,
34190
3
The Office of Primary Industries and Mines Region 3, Chiang Mai, 50200 Thailand.
Correspondence author: kkerdsiri @ hotmail.com
The concentrations of zinc cadmium and lead in contaminated soils, field soil samples used for this
study was collected from the zinc mine in the Mae Sod district at Tak Province, Thailand,
were determined by flame atomic absorption spectrometry (FAAS) using the modified BCR (the
European Community Bureau of Reference) sequential extraction procedure. A three stages sequential
extraction procedure, i.e. acid – extractable fraction (0.11 mol/l acetic acid), iron and manganese
oxides bound (0.1 mol/l hydroxylamine hydrochloride, pH 2), organic matter bound (30% hydrogen
peroxide acidified to pH 2.0 with nitric acid followed by extraction with 1.0 mol/l ammonium acetate
pH 2), sequentially. The residual were digestion with aqua regia. The results show that, zinc and
cadmium were mostly found in the acid – extractable fraction and lead was mostly found in the
residual fraction of the contaminated soils. The mobility based on the sum of the BCR sequential
extraction stages was: cadmium (95%) > zinc (62%) > lead (47%). Percentage recoveries by
sequential extraction procedure were found to be 98.7, 100.4 and 102.0 for zinc cadmium and lead
respectively. Relative standard deviation of procedure was usually lower 9% (n=7).
Key words: Zinc, Cadmium, Lead, Contaminated soil, BCR sequential extraction
Cadmium conference 2010
51
Screening of CadmiumCadmium-Resistant Microorganisms
from Soil of MaeMae-Sod, Tak
Wassana Chatdumrong, Phungphet Waree and Srisuda Kawayasakul
Department of Microbiology and Parasitology, Faculty of Medical Science, Naresuan University.
Phitsanulok, Thailand.
Correspondence author: Wassana_c@yahoo.com
Eleven soil samples were collected from 3 areas of Mae Sod district, Tak province. The highest
cadmium (Cd) contaminated soil (49.008 mg/kg) were found in the samples from Padae village. Most
of the samples contained total microorganisms in a range of 106-107 cfu/g and pH between 5.41-7.53.
The screening study on the 100 mg/l Cd agar had found bacteria, fungi and yeast at 37, 84 and 16
isolates, respectively. However, only 11 bacterial isolates (29.73%) resisted to Cd at 200 mg/l
whereas 42 fungal isolates (50%) and 5 isolates (31.25%) of yeast showed higher resistance to Cd at
400 mg/l. The fungal isolate no.3.1.1 was able to grow to 2.3 cm in diameter even on 1,000 mg/l Cdmedium. All of the 11 bacterial isolates showed similar morphological and biochemical properties.
However, the bacterial isolate no. 1.3.4 could growth to the highest Cd concentration at 200 mg/l in
medium broth. The fungal isolate no. 3.1.1 and the bacterial isolate no. 1.3.4 will be further identified
their strains by molecular techniques and investigated their Cd-biosorption efficiency.
Keywords: microorganisms, cadmium, resistant
Cadmium conference 2010
52
Heavy metals in dust fall in Phitsanulok
Phitsanulok Areas
Khwanruthai Thongboonyalith and Pajaree Thongsanit
Department of Civil Engineering, Faculty of Engineering, Naresuan University ,Muang, Phitsanulok
Thailand,65000
Correspondence author: pajareethongsanit@yahoo.com
The heavy metals concentrations in dust fall in Phitsanulok area were studied in April 2009 and
November 2009. The four sample sites were Naresuan University Secondary Demonstration School
site; the roadside building at Banklong intersection area site; the Buddhachinarajphittaya School site
and the roadside building at Makro shopping center intersection area site. The dust falls jars were set
on the top of buildings, 15 meter from the ground level. The dust samples were collects every 30 days.
The dust fall levels were found vary from the minimum value 3.74 mg/m2/day at Naresuan University
Secondary Demonstration School site in April 2009 to a maximum of 175.64 mg/m2/day at
Banklong site in April 2009. The dust fall concentrations were high at roadside building sites. It was
indicated that the some dust fall data were higher than the standard residential area (65-130
mg/m2/day). The heavy metal concentrations were analyzed via Atomic Absorption
Spectrophotometer (AAS). It was found that the third orders of the maximum metal concentration are
Iron, Zinc and Manganese, respectively. The manganese concentrations were vary from 0.0007 to
0.0115 mg/m2/day.
Keywords: Heavy metal; Dust fall; Phitsanulok
Cadmium conference 2010
53
LIST OF INVITED
SPEAKERS
SPEAKERS
Cadmium conference 2010
54
List of Invited Speakers
Arora Manish, Ph.D.
Environmental and Occupational Medicine
and Epidemiology,
Harvard School of Public Health,
677 Huntington Avenue, Boston 02115,
Massachusetts, USA
Population Oral Health,
Faculty of Dentistry,
University of Sydney,
1 Mons Road, Westmead 2145,
New South Wales, AUSTRALIA
e-mail: marora@hsph.harvard.edu
Bandara J.M.R.S. Ph.D.
Professor
Department of Agriculture Biology,
University of Peradeniya,
Peradeniya, SRI LANKA
Board of Study in Plant Protection, PGIA,
University of Peradeniya,
Peradeniya SRI LANKA
e-mail: bandara.sarath@gmail.com
Fowler A Bruce, Ph.D.
Division of Toxicology and Environmental
Medicine, ATSDR
Atlanta, GA, USA
e-mail: bxf9@cdc.gov
Gobe Glenda, M.D., Ph.D
Associate Professor
Centre for Kidney Disease Research,
University of Queensland School of Medicine,
Princess Alexandra Hospital, Woolloongabba,
Brisbane, AUSTRALIA
e-mail: g.gobe@uq.edu.au
Ha Quang Pham, Ph.D.
Associate Professor
Institute for Agricultural Environment
(IAE/VAAS) Phu Do, Tu Liem,
Hanoi, VIETNM
e-mail: pqha-nisf@hn.vnn.vn
Hipkaeo Wiphawi, Ph.D.
Assistant Professor
Department of Anatomy,
Faculty of Medical Science,
NaresuanUniversity, Phitsanulok 65000
THAILAND
e-mail: hipkaeo1@hotmail.com
Jinayon Sujin, Ph.D.
Professor
President of Naresuan University
Phitsanulok, THAILAND
Kikuchi Mihoko, Ph.D.
Senior Assistant Professor
Center of International Collaborative
Research, Nagasaki University, Nagasaki,
JAPAN
e-mail: mkikuchi@nagasaki-u.ac.jp
Landolph R Joseph, Jr, Ph.D
Associate Professor
Department of Molecular
Microbiology/Immunology and Pathology,
USC Cancer Center, Keck School of
Medicine, Univ. Southern California, Los
Angeles, California, 90033, USA
e-mail: landoph@usc.edu
Nilesh M. Kalariya, Ph.D.
Department of Ophthalmology & Visual
Sciences, University of Texas Medical Branch,
Galveston, TX 77555, USA
e-mail: nmkalari@utmb.edu
Satarug Soisungwan, Ph.D.
Professor
National Research Centre for Environmental
Toxicology, Brisbane, Queensland,
AUSTRALIA
Visiting Research Professor, Pathology
Department, University of North Dakota
School of Medicine and Health Sciences,
Grand Forks, ND 58202, USA
e-mail: ssatarug@medicine.nodak.edu
Supanpaiboon Wisa, Ph.D.
Department of Biochemistry,
Faculty of Medical Science,
Naresuan University, Phitsanulok 65000
THAILAND
e-mail: supanpaibon@yahoo.com
Suwazono Yasushi. M.D., Ph.D.
Professor
Department of Occupational and
Environmental Medicine, Graduate School of
Medicine, Chiba University, 1-8-1 Inohana,
Chuoku, Chiba 260-8670 JAPAN
e-mail: suwa@faculty.chiba-u.jp
Thevenod Frank, M.D., Ph.D.
Professor
University of Witten/Herdecke,
Inst Phsyiol/Pathophsyiol Medizinische,
Stockumer Str 12 (Thyssenhaus),
D-58448 Witten, GERMANY
e-mail: frank.thevenod@uni-wh.de
Vahter Marie. Ph.D.
Professor
Institute of Environmental Medicine,
Karolinska Institutet,
Stockholm, SWEDEN
e-mail: Marie.Vahter@ki.se
Vesey A David, Ph.D.
Senior Research Scientist
Centre for Kidney Disease Research (CKDR),
The University of Queensland,
Princess Alexandra Hospital, Brisbane,
Queensland 4102, AUSTRALIA
e-mail: david_vesey@health.qld.gov.au
Warne Michael, Ph.D.
Principal Research Scientist
Commonwealth Scientific and Industrial
Research Organisation (CSIRO) Clayton
South VIC 3169, AUSTRALIA
e-mail: michael.warne@csiro.au
Cadmium conference 2010
56
LIST OF
PARTICIPANTS
Cadmium conference
conference 2010
57
List of Invited Speakers
Arora Manish, Ph.D.
Environmental and Occupational Medicine
and Epidemiology,
Harvard School of Public Health,
677 Huntington Avenue, Boston 02115,
Massachusetts, USA
Population Oral Health,
Faculty of Dentistry,
University of Sydney,
1 Mons Road, Westmead 2145,
New South Wales, AUSTRALIA
e-mail: marora@hsph.harvard.edu
Bandara J.M.R.S. Ph.D.
Professor
Department of Agriculture Biology,
University of Peradeniya,
Peradeniya, SRI LANKA
Board of Study in Plant Protection, PGIA,
University of Peradeniya,
Peradeniya SRI LANKA
e-mail: bandara.sarath@gmail.com
Fowler A Bruce, Ph.D.
Division of Toxicology and Environmental
Medicine, ATSDR
Atlanta, GA, USA
e-mail: bxf9@cdc.gov
Gobe Glenda, M.D., Ph.D
Associate Professor
Centre for Kidney Disease Research,
University of Queensland School of Medicine,
Princess Alexandra Hospital, Woolloongabba,
Brisbane, AUSTRALIA
e-mail: g.gobe@uq.edu.au
Ha Quang Pham, Ph.D.
Associate Professor
Institute for Agricultural Environment
(IAE/VAAS) Phu Do, Tu Liem,
Hanoi, VIETNM
e-mail: pqha-nisf@hn.vnn.vn
Hipkaeo Wiphawi, Ph.D.
Assistant Professor
Department of Anatomy,
Faculty of Medical Science,
NaresuanUniversity, Phitsanulok 65000
THAILAND
e-mail: hipkaeo1@hotmail.com
Jinayon Sujin, Ph.D.
Professor
President of Naresuan University
Phitsanulok, THAILAND
Kikuchi Mihoko, Ph.D.
Senior Assistant Professor
Center of International Collaborative
Research, Nagasaki University, Nagasaki,
JAPAN
e-mail: mkikuchi@nagasaki-u.ac.jp
Landolph R Joseph, Jr, Ph.D
Associate Professor
Department of Molecular
Microbiology/Immunology and Pathology,
USC Cancer Center, Keck School of
Medicine, Univ. Southern California, Los
Angeles, California, 90033, USA
e-mail: landoph@usc.edu
Nilesh M. Kalariya, Ph.D.
Department of Ophthalmology & Visual
Sciences, University of Texas Medical Branch,
Galveston, TX 77555, USA
e-mail: nmkalari@utmb.edu
Satarug Soisungwan, Ph.D.
Professor
National Research Centre for Environmental
Toxicology, Brisbane, Queensland,
AUSTRALIA
Visiting Research Professor, Pathology
Department, University of North Dakota
School of Medicine and Health Sciences,
Grand Forks, ND 58202, USA
e-mail: ssatarug@medicine.nodak.edu
Supanpaiboon Wisa, Ph.D.
Department of Biochemistry,
Faculty of Medical Science,
Naresuan University, Phitsanulok 65000
THAILAND
e-mail: supanpaibon@yahoo.com
Suwazono Yasushi. M.D., Ph.D.
Professor
Department of Occupational and
Environmental Medicine, Graduate School of
Medicine, Chiba University, 1-8-1 Inohana,
Chuoku, Chiba 260-8670 JAPAN
e-mail: suwa@faculty.chiba-u.jp
Thevenod Frank, M.D., Ph.D.
Professor
University of Witten/Herdecke,
Inst Phsyiol/Pathophsyiol Medizinische,
Stockumer Str 12 (Thyssenhaus),
D-58448 Witten, GERMANY
e-mail: frank.thevenod@uni-wh.de
Vahter Marie. Ph.D.
Professor
Institute of Environmental Medicine,
Karolinska Institutet,
Stockholm, SWEDEN
e-mail: Marie.Vahter@ki.se
Vesey A David, Ph.D.
Senior Research Scientist
Centre for Kidney Disease Research (CKDR),
The University of Queensland,
Princess Alexandra Hospital, Brisbane,
Queensland 4102, AUSTRALIA
e-mail: david_vesey@health.qld.gov.au
Warne Michael, Ph.D.
Principal Research Scientist
Commonwealth Scientific and Industrial
Research Organisation (CSIRO) Clayton
South VIC 3169, AUSTRALIA
e-mail: michael.warne@csiro.au
Cadmium conference 2010
56
LIST OF
PARTICIPANTS
Cadmium conference
conference 2010
57
List of Participants
Boonchalearmkit Sukanya
Department of Environmental Quality Promotion
49 Rama VI soi 30, Phayathai Bangkok10400
THAILAND
e-mail: sukanya@deqp.go.th
Boonlert Wanvisa
Department of Medical Technology
Faculty of Allied Health Science,
Naresuan University
Phitsanulok 65000 THAILAND
e-mail: wanvisaboon@yahoo.com
Boonsong Tantip
Department of Biochemistry,
Faculty of Medical Science, NaresuanUniversity,
Phitsanulok 65000 THAILAND
e-mail: tantips@hotmail.com
Bualeong Tippaporn
Department of Physiology
Faculty Medical Science
Naresuan University, THAILAND
e-mail: tippapornb@nu.ac.th
Buddhanbut Somrit
Office of the Reverse Brain Drain Project,
NSTDA 111 Paholythin Rd., Klong 1,
Klong Luang. Pathumthani 12120 THAILAND
Tel : 66-2-5647000, Ext. 1446-1448;
Fax : 66-2-5647004
e-mail: somrit@nstda.or.th
Chantaraprathet Narissara
Department of Biochemistry,
Faculty of Medical Science, NaresuanUniversity,
Phitsanulok 65000 THAILAND
e-mail: miwnaka_123@hotmail.com
Cheunchoojit Supaporn
Department of Community Health, Faculty of
Sciences, Burirum Rajabhat University, Burirum
31000 THAILAND
Chootip Krongkarn
Department of Physiology
Faculty Medical Science
Naresuan University, THAILAND
e-mail: krongkarnc@nu.ac.th
Chumark Pilaipark
Department of Cchemistry
Faculty of Sciences
Naresuan University
Pitsanulok, THAILAND
e-mail: pilaiparkc@nu.ac.th
Funkhiew Thippawan
Mae-sot hospital ,Mae-sot ,Tak
63110 THAILAND
Jaiyasit Nuntana
Phatadphadang Health Station,
Phatadphadang, Mae Sot, Tak 63110
THAILAND
Jawanna Nongnad
Mae Ku Nhau Public Health Center, Mae Ku
Nhau, Mae Sot, Tak 63110 THAILAND
Juntarawijit Chudchawal
Department of Natural Resources and
Environmen, Faculty of Agriculture Natural
Resources and Environment
Naresuan University, Phitsanulok 65000
THAILAND
e-mail: chudchawalj@gmail.com
Kalayanukoul Kitisil
CTI Tower, 26th-27th Floor,191/18-25
Ratchadaphisek road,
Khlong Toei , Bangkok 10110, THAILAND
e-mail: kitisilk@padaeng.co.th
Kanluan Taweesook
NaresuanUniversity, Phitsanulok 65000
THAILAND
Kaoropcroo Nitima, Captain
Food and Water Sanitation Divition
Department of Health, Ministry of Public Health,
Nonthaburi 11000 THAILAND
e-mail: nitima@rocketmail.com
Khongsombat Onrawee
Department of Physiology
Faculty Medical Science
Naresuan University, THAILAND
e-mail: onraweek@nu.ac.th
Kongngoen Sukanya
Bureau of Rice research and Development
Phahon Yothin Road ,
Jatujak, Bangkok, THAILAND 10900
e-mail: sukanya@brrd.in.th
Krongyut Sutankamol
Department of Anatomy,
Faculty of Medical Science, NaresuanUniversity,
Phitsanulok 65000 THAILAND
Kumchatuek Tewarat
Depaertment of Anatomy, Faculty of Medical
Sciences, Naresuan University ,Pitsanulok
THAILAND
e-mail: tewarat@hotmail.com
Lhaaub Arun
Mae Tao Health Station, Mae Tao, Mae Sot,
Tak 63110
THAILAND
Limmongkol Apinan
Assistant Dean for Stadent Affairs
Faculty of Medical Science
Naresuan Univesity Pitsanulok, THAILAND
e-mail: apinunl@hotmail.com
Limwongse Wisaka
Naresuan University, Phitsanulok 65000
THAILAND
Mahasakpunt Pranee
Mae-sot hospital ,Mae-sot ,Tak
63110 THAILAND
Malakul Wachirawadee
Department of Physiology
Faculty of Medical Science
Naresuan University
Pitsanulok, THAILAND
e-mail: wachirawadeem@hotmail.com
Namvongsakool Poonikha
Depaertment of Anatomy, Faculty of Medical
Sciences, Naresuan University ,Pitsanulok
THAILAND
e-mail: poonikhan@nu.ac.th
Nak-ung Sureeporn
Department of Anatomy
Faculty Medical Science
Naresuan University, THAILAND
e-mail: som.art@live.com
Ngourungsi Kanchana
NaresuanUniversity, Phitsanulok
65000 THAILAND
e-mail: kanchana19@yahoo.com
Noomkleng Sucha
Department of Biochemistry
Faculty of Medical Science
Naresuan University, THAILAND
e-mail: cha_medsci@hotmail.com
Norkaew Thongchai
Department of Biochemistry,
Faculty of Medical Science, NaresuanUniversity,
Phitsanulok 65000 THAILAND
e-mail: look4thong@hotmail.com
Pansiri Sirima
Bureau of Rice research and Development
Phahon Yothin Road ,
Jatujak, Bangkok, THAILAND 10900
e-mail: sukanyak@hotmail.com
Pasurivong Orapin
Department of Physiology
Faculty of Medicine
Khon Kaen University
Khon Kaen, THAILAND
e-mail: orapin@kku.ac.th
Peanomlom Pongpot
Mae-sot hospital, Mae-sot ,Tak
THAILAND 63110
Phuapittayalert Laorrat
Department of Anatomy
Faculty Medical Science
Naresuan University, THAILAND
e-mail: picki_picky@hotmail.com
Pimolsri Lee Urat
Department of Faculty of Medical
ScienceNaresuan University
Pitsanulok, THAILAND
e-mail: uratp@yahoo.com
Polseela Raxsina
Faculty of Medical Sciences
Naresuan University
Pitsanulok, THAILAND
e-mail : polseela@hotmail.com
Prawantao Wirat
Office of Diseases Prevention and Control 9
Pitsanulok
e-mail: virat-99@hotmail.com
Pumchoe Cawaphorn
Bureau of Rice research and Development
Phahon Yothin Road Jatujuk, Bangkok,
THAILAND 10900
e-mail: cawaphorn_p@hotmail.com
Puntheeranurak Supaporn
Department of Physiology
Faculty Medical Science
Naresuan University, THAILAND
e-mail: supapornp@nu.ac.th
Pupatwibul Kanungnit
NaresuanUniversity, Phitsanulok
65000 THAILAND
e-mail: kanungnitp@nu.ac.th
Putiwat Phongpitak
Depaertment of Anatomy,
Faculty of Medical Sciences, Naresuan
University ,Pitsanulok ,THAILAND
e-mail : phongpitakp@hotmail.com
Sakulsak Nattiya
Department of Anatomy,
Faculty of Medical Science, NaresuanUniversity,
Phitsanulok 65000 THAILAND
e-mail : nsakulsak@yahoo.com
Sawasdidoln Chakrit
Assistant Dean for Academic Quality Assurance
Faculty of Medical Science
Naresuan Univesity Pitsanulok, THAILAND
e-mail: sawasdidoln_chakrit@ hotmail.com
Seang-Ananta Karn Pisid
Department of Anatomy,
Faculty of Medical Science, NaresuanUniversity,
Phitsanulok 65000 THAILAND
e-mail: pisidsang@hotmail.com
Siriked Ketsarin
Department of Anatomy
Faculty of Medical Science
Naresuan University, THAILAND
e-mail: beerchan1@hotmail.com
Somsuan Keerakarn
Department of Anatomy,
Faculty of Medical Science, NaresuanUniversity,
Phitsanulok 65000 THAILAND
e-mail : kee_kyopt@hotmail.com
Sriaium Jukkrit
Public Health Center, Mae Sot, Tak
63110 THAILAND
Srisawang Piyarat
Faculty of Medical Science
Naresuan University
Pitsanulok, THAILAND
e-mail: piyarats@nu.ac.th
Sudsaward Sangkab
Depaertment of Anatomy, Faculty of Medical
Sciences, Naresuan University ,Pitsanulok
THAILAND
e-mail: sangkab@hotmail.com
Suphagosol Kowit
Department of Physiology
Faculty Medical Science
Naresuan University, THAILAND
e-mail: kowits@nu.ac.th
Syers Keith J.
NaresuanUniversity, Phitsanulok 65000
THAILAND
e-mail: keiths@nu.ac.th
Taepavarapruk Pornnarin
Head of department of Physiology
Faculty of Medical Science
Naresuan Univesity Pitsanulok, THAILAND
e-mail : Taepavap@yahoo.com
Tanpipat Noppawan
Assistant President of NSTDA
Office of the Reverse Brain Drain Project,
NSTDA
111 Paholythin Rd., Klong 1,Klong Luang.
Pathumthani 12120 THAILAND
Tel : 66-2-5647000, Ext. 1446-1448;
Fax : 66-2-5647004
e-mail: noppawan.tanpipat@nstda.or.th
Tangpong Jitbanjong
Assistant Professor
School of Allied Health Sciences and Public
Health
Walailak University, Nakhon Si Thammarat
80160 THAILAND
e-mail: rjitbanj@wu.ac.th
Techakitiroj Chatkul
Department of Biochemistry and Microbiology
Faculty of Pharmaceutical Sciences
Chulalongkorn university
e-mail: tverakit@gmail.com
Thongchub Winai
Office of Diseases Prevention and Control 9
Pitsanulok
e-mail: winai_dpc9@hotmail.com
Thongkamsuk Thanoo
Bureau of Dug and Narcotic, Department of
Medical sciences, Ministry of Public Health,
Nonthaburi 11000 THAILAND
e-mail : keenoo100@hotmail.com
Thongrod Nuchareeporn
Department of Anatomy,
Faculty of Medical Science, NaresuanUniversity
Phitsanulok 65000 THAILAND
Thongsanit Pajaree
Department of Civil Engineering
Faculty of engineering
Naresuan University ,Pitsanulok ,THAILAND
pajareethongsanit@yahoo.com
Tiangyou Watcharee
Department of Anatomy,
Faculty of Medical Science, NaresuanUniversity,
Phitsanulok 65000 THAILAND
e-mail: twatcharee@hotmail.com
Tongpob Yutthapong
Department of Anatomy,
Faculty of Medical Sciences, Naresuan
University ,Pitsanulok THAILAND
e-mail : yutthapongt@nu.ac.th
Tungkananukulchai Unnop
CTI Tower, 26th-27th Floor,191/18-25
Ratchadaphisek road,
Khlong Toei , Bangkok 10110, THAILAND
e-mail: unnopt@padaeng.co.th
Vitta Apichat
Department of Microbiology and Parasitology,
Faculty of Medical Science, Naresuan University
THAILAND
e-mail: apichatvitta@hotmail.com
NaresuanUniversity, Phitsanulok 65000
THAILAND
e-mail: detw@nu.ac.th
Wasuntarawat Chanchira
Department of Physiology,
Faculty of Medical Science, NaresuanUniversity,
Phitsanulok 65000 THAILAND
e-mail: w_chanchira@hotmail.com
Wichai Siriwan
Department of Microbiology and Parasitology,
Faculty of Medical Science, NaresuanUniversity,
Phitsanulok 65000 THAILAND
e-mail: siriwanw@nu.ac.th
Wongwilairat Rosarin
Department of Microbiology and Parasitology,
Faculty of Medical Science, NaresuanUniversity,
Phitsanulok 65000 THAILAND
e-mail: rosarinw@nu.ac.th
Wuthichotwanichgij Gobchok
Office of Diseases Prevention and Control 9
Pitsanulok
e-mail: gobchoke@hotmail.com
Wattanachaiyingcharoen Det
Yanlap Witaya
Head of Secretary of the Faculty of Medical
Science Naresuan Univesity, THAILAND
e-mail : w_yanlaph@hotmail.com
Yapeng Taewicha
Mae Ku Public Health Center, Mae Ku,
Mae Sot, Tak 63110
THAILAND
Yasothornsrikul Sukkid
Department of Biochemistry,
Faculty of Medical Science, NaresuanUniversity,
Phitsanulok 65000 THAILAND
e-mail: sukkidy@nu.ac.th
Yingsukpisarn Surawud
Department of Physiology
Faculty of Medical Science
Naresuan University
Pitsanulok, THAILAND
e-mail: organon999@yahoo.com
Boonthum Ratchaneekorn
Regional Medical Sciences center
Phitsanulok, Phitsanulok 65000 THAILAND
e-mail : R_unun@hotmail.com
Donpunha Wanida
Department of Physiology
Faculty of Medicine
Khon Kaen University
Khon Kaen, 40002 THAILAND
e-mail : wanida_ams@yahoo.com
Kukongviriyapan Upa
Department of Physiology
Faculty of Medicine
Khon Kaen University
Khon Kaen, 40002 THAILAND
e-mail : upa_ku@kku.ac.th
Megwanit Surapol
Sirindhorn college of public health chonburi,
Chonburi 20000 THAILAND
e-mail : suratao@hotmail.com
Pakdeechote Poungrat
Department of Physiology
Faculty of Medicine
Khon Kaen University
Khon Kaen, 40002 THAILAND
e-mail : ppoung@kku.ac.th
Phaisansuthichol Sirirat
Department of Chemistry, Faculty of Science,
Maejo University, Chiangmai 50290
THAILAND
e-mail : phaisansuthichol@gmail.com
Rithiudom Sumalee
Regional Medical Sciences center
Phitsanulok, Phitsanulok 65000 THAILAND
e-mail : sumalee.r@dmsc.mail.go.th
Sataruksa Oungsakul Peangjai
Khon Kaen, 40002 THAILAND
e-mail : peaoun@kku.ac.th
Scholfield C Norman
Department of Physiology,
Naresuan University, Phitsanulok 65000
THAILAND
e-mail : CNS@post.com
Sompamit Kwanjit
Department of Physiology
Faculty of Medicine
Khon Kaen University
Khon Kaen, 40002 THAILAND
e-mail : k_kwanjit@yahoo.com
Cadmium conference 2010
62
SPONSORS AND
CONTRIBUTORS
Cadmium conference 2010
63
Thank you message
to sponsors
On the behalf of the organizing committee of the “Reverse Brain Drain Project
(RBD-NSTDA) Special Conference Cadmium in Food and Human Health
&Technologies for Environmental Restoration and Rehabilitation at Phitsanulok
during January 15-17, 2010, we would like to extend sincere thanks to our
sponsors for the supports. We really do appreciate your gracious generosity.
Cadmium conference 2010
64
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Vission/Mission
NSTDA:
A Driving Force for National Science and Technology Capacity
VISION
A key partner in developing a knowledge-based society through the application of science and technology
MISSION
Research and development to strengthen Thailand's sustainable competitiveness, complemented by
technology transfer and the development of human resources and science and technology infrastructure,
with outcomes that have positive impacts on society and the economy.
CORE VALUES
NSTDA embraces five core values as guiding principles to ensure performance excellence and efficient
interaction within NSTDA.
NSTDA core values are:
N = Nation First
S = S & T Excellence
T = Teamwork
D = Deliverability
A = Accountability