Body Burden- Pesticide residues

Pesticide Residues Impact on Health and Detection
Pesticides are important input to modern agriculture and also used in public health in controlling
communicable disease. The toxicity of these compounds poses risk to human health, environment and
to the organisms which may not be targeted by pesticides. The effect of pesticides and their mobility
depend upon their chemical and physical properties, soil characteristics, groundwater infiltrations and
vadose zone behaviour, vegetation and local weather conditions. They resist degradation by chemical,
physical or biological means. “There is no sort of lower standard or different standard used for
pesticide products,” says Angus Cameron, a former manager of the firm Inveresk Research International
in Scotland, where many of the human tests have been conducted.
Pesticide residues present in food are due to:
‧ Direct use of pesticide on the food crop;
‧ animal feeding on pesticide contaminated feed;
‧ environmental contamination and Adulteration.
The total intake of organochloride pesticides such as DDT, aldrin,dieldrin, hexachloro benzene
etc.,through food is 223 microgrammes per person per day in India. In comparison the same is only 3.8
microgrammes per person per day in the United States. Most fruit and vegetables are grown using
pesticides. Their widespread usage is causing health problems due to residues of pesticides in food and
pollution of drinking water.
The most worrying types of chemicals are those which are hormone disrupters and which can build up
inside the human body. Hormone disrupters interfere with our body’s hormones. Our hormones
regulate our day-to-day bodily functions and are vital for making sure we grow up healthy.
Some chemicals that we can’t break down properly will accumulate in the body’s tissues. This is known
as bioaccumulation. Safeguards for pesticides in food do not contain much-needed special protections
for infants and children. Instead they are geared to the “average” person in the population.
Organophosphates, tend to break down so rapidly that they are unlikely to show up on food unless
applied to crops very close to harvest time, but they are often more acutely toxic.
In India, a 7-year study showed that organochlorine residues were above the tolerance limits in more
than 35 percent of the food. While exported foods are usually monitored carefully so that they will
pass the inspections locally marketed foods are usually not monitored, yet these are most likely to
have residues of the short-lived, highly toxic organophosphates because of the short time between
harvesting and marketing.
Eating ‘safe’ means calculating what we eat, how much we eat and how much pesticide can be allowed
in what we eat. The food basket is also our pesticide basket. We have to ingest pesticides because we
need nutrition, but we must not exceed our quota of pesticides that is allowed or acceptable. You can
call this the nutrition-poison trade-off. So long as we cannot wish away pesticide use, it is imperative
that this trade-off is a prudent one. But if the food has no nutritive value and carries poisonous
pesticides with it, consuming even the smallest possible amount would be unsafe because the body will
only get the poison and not its antidote, the nutrition. This is the whole logic behind pesticide health
risk management. Currently, the pesticide intake through an Indian diet exceeds the ADIs of the
commonly used pesticides.
Maximum Residue Levels of Pesticides in Food
1. In order to protect the health of the consumer while facilitating international trade, the Codex
Alimentarius Commission (Codex) has established Maximum Residue Limits (MRLs) for individual
pesticides in selected commodities. MRL is the maximum concentration of a pesticide residue to be

permitted in a food commodity. The primary objective of setting MRLs is to protect the health of
consumer by ensuring that only the minimum amount of pesticide is applied to food for achieving the
actual pest control needs.
2. Codex MRLs are established on the basis of appropriate residue data obtained mainly from
supervised field trials. Supervised trials are scientific studies in which pesticides are applied to crops or
animals in the way which is intended to reflect commercial practice according to Good Agricultural
Practice (GAP). GAP in the use of pesticides includes the authorised safe use of pesticides under actual
conditions necessary for effective and reliable pest control and in a manner which leaves a residue
which is the smallest amount practicable.
3. Even though the primary purpose of setting MRLs in food is to protect the health of consumers and
the levels are intended to be toxicologically acceptable (i.e. do not cause acute or chronic toxicities in
humans), it should not be confused with safety limits which are expressed in terms of the Acceptable
Daily Intake (ADI) of a particular pesticide residue from all sources. It follows that exposure to
pesticide residues in excess of MRLs does not automatically imply a hazard to health. Instead, a
residual level exceeding the MRL is more a reflection for non-compliance to GAP.
4. for some pesticides that have been banned or are no longer in use, trace amount of their residues
and metabolites may be present in food as environmental contaminants because of their persistence in
nature. Codex has established "extraneous maximum residue limits" (EMRLs) for some of these
persistent pesticides. EMRL refers to residues of compounds, once used as pesticides but are not any
more registered as pesticides, arising from environmental contamination.
Pesticides Detected
Pesticides have been found in human blood, urine, breast milk, semen, adipose
tissue, amniotic fluid, infant meconium and umbilical cord blood. Cumulative exposure to pesticides
may come from food, water, air, dust, soil etc. Pesticides can be absorbed through skin contact,
inhalation or accidental ingestion. Organochlorine and Organophosphorus pesticides are most
commonly found Food residues.
Permissible limits in Human body
Depending on the nature of individual pesticide, the amount and duration of exposure, pesticides
exceeding safety limits may cause acute and/or chronic effects in humans.
1.Adverse health effects include damage to nervous system or other organs such as the liver
and kidneys. Some may be transferred via the placenta or breast feeding, thereby affecting the
foetal development.
2. The ADI of a chemical is the estimate of the amount of a substance in food or drinking-
water, expressed on a body-weight basis, that can be ingested daily over a lifetime without
appreciable health risk to the consumer on the basis of all the known facts at the time of the
evaluation.
3. A dietary intake above the ADI does not automatically mean that health is at risk. Transient
excursion above the ADI would have no health consequences provided that the average intake
over long period is not exceeded as the emphasis of ADI is a lifetime exposure.
So how safe is the food?
"Food safety" implies absence or acceptable and safe levels of contaminants, adulterants,
naturally occurring toxins or any other substance that may make food injurious to health on an
acute or chronic basis. We are what we eat. Our nutritional status, health, physical and mental

faculties depend on the food we eat and how we eat it. Food contamination can take place at
various stages of the food chain from farm to table. Apart from chemical contamination of food
from various sources such as industries, vehicles, pesticides and fertilizers, pollution resulting
from growing of vegetables in degraded environmental conditions in peri-urban zones also
affects food safety. This is coupled with further pollution from vehicles and industries during
marketing. The common sources include presence of heavy metals, pesticides, preservatives,
colouring agents and other additives and adulterants in food.
Pesticide: a Lurking Menace
India uses about 30,000 tons of pesticides a year, more than 60% of it on food crops. Use of excessive
pesticides contaminates soil, water and finally enters the food chain and contaminates the food
produced. About 20% of Indian food products contain pesticide residues above the tolerance level
compared to only 2% globally. No detectable residues are found in only 49% Indian food products
compared to 80% globally. The UNEP estimates accidental pesticide poisoning causing 20,000 deaths
and 1 million cases of illness per year worldwide. Pesticides have been implicated in human studies
with leukemia, lymphoma, aplastic anemia, soft tissue sarcoma and cancers of the breast, brain,
prostate, testis and ovaries. The International Agency for Research on Cancer has found "sufficient"
evidence of carcinogenic potentiality in most of the pesticides beyond the threshold limit.
Impact on crossing safe limit – Diseases
The prescribed Acceptable Daily Intake (ADI) and Maximum Residue Limit (MRL) for India is being
determined based on the recommendation of the Codex Committee on Pesticides Residues (CCPR) a
subsidiary body of the Codex Alimentarius Commission. Acceptable Daily Intake or ADI is a measure of
the amount of a specific substance (usually food adititive or pesticide) in food that can be ingested
(orally) over a lifetime without an appreciable health risk. Without appreciable risk" refers to the
practical certainty that injury will not result, even after a lifetime of experience. ADIs are expressed
by body mass, usually in milligrams (of the substance) per kilograms of body mass per day. The concept
of ADI was first introduced in 1961 by the Coucil of Europe and later the Joint Expert Commiitee on
Food Additives (JECFA), a commiitee maintined by two United Nations bodies: the Food and
Agricultural Organisations and WHO.
Maximum Residue Limits or MRL for pesticides are established in most countries to safeguard consumer
health and to promote GAP in the use of insecticides, fungicides, herbicides and other agricultural
compounds. MRL is the maximum concentration of a substance, expressed in milligrams per kilogram
(parts per million, ppm) or in micrograms per kilogram (parts per billion, ppb) that is legally permitted
in a food commodity. An MRL is typically applied to a veterinary drug or a pesticide and is established
for particular food commodities such that potential consumer exposure to residues is judged to be
toxicologically acceptable. The MRL set for a substance may differ for different food commodities,
reflecting the contribution of the particular food to a "standard" diet. Normal intake of food containing
residue of a substance at its MRL is not expected to result in the ADI being exceeded.
Reasons for more Pesticide residues in India
The pesticides are used improportionately in India in relation to places and the amount of pesticides
residue varies from one place to another. Tamil Nadu consumes 1.2-2.0 kg/ha of land followed by
Andhra Pradesh and Punjab where 0.8-1.2 kg is the rate of consumption. Pesticide residues in the feed
and fodder are solely responsible for their accumulation in animal and poultry. The states like
Tamilnadu, AP, Punjab, Haryana, and Karnataka have highest use of pesticides in order to get more
production while on the other hand the states like Bihar, West Bengal, North eastern states have

lowest use of pesticides. It is because of illiteracy of farmers, poor economic conditions or due to lack
of awareness. So the food commodities in high using states have more residues of pesticides.
Status of pesticide residues in India
The presence of pesticide residues have been detected in various items and in food chain. The levels of
the pesticides are found much higher than expected because of heavy contamination of environment.
Besides, there are human milk, fat or tissue samples screened for the presence of pesticide residues
were also found to have very significant levels of harmful pesticides. The BHC has been found from
0.120 to 1.22 PPM in human fat samples. Heptachlor, an organochlorine pesticide was found to be
0.425 PPM and DDT from 0.195 to 1.695 PPM. Even human breast milk is not free from DDT, which was
found to have even 2.39 PPM levels. Similarly human blood was found to have a much higher
concentration of 12.00 PPM as against of 0.050-PPM safe levels (no effect levels).
Another classification of pesticides from the World Health Organisation, is as per their acute toxicity.
This classification includes Class I a – Extremely hazardous, demarcated in red; Class I b – Highly
Hazardous, symbolized by an yellow triangle; Class II – Moderately Hazardous, marked by a blue
triangle; Class III is known as Slightly Hazardous; while the remaining class is supposed to be Not likely
to be Hazardous. It is to be noted here that two thirds of the pesticides consumed in India fall under
WHO Class I and II pesticides.
Between 1965 and 1998, the contamination of food from pesticides in India has been estimated at only
41% being free from residues, as compared to 63% being free from residues that 20% of the
contamination is above fixed Maximum Residue Limits [MRLs]. In the EU, this is estimated to be only
around 1.4% while in the USA, in 1996, it is reported that the contamination above MRLs was around
4.8%. In the 1980s, the All India Coordinated Research Project on Pesticide Residues (AICRPPR) was set
up to monitor pesticide residues all over the country.In 1999, the AICRPPR reported that, with all
commodities put together, 20% of the food samples tested exceeded the MRLs. Fruits, vegetables and
milk are found to be highly contaminated. Monocrotophos, Methyl Parathion and DDVP, all organo
phosphorus pesticides, are found to be most prevalent. These are also WHO Class I pesticides.
The pesticide detection rate for green leafy vegetables during winter months was 53.3% as compared
to
those of rainy (8.3%) and summer months (23.1%). Corresponding figures for non-leafy vegetables were
30%, 12.5% and 19.5%, respectively (Mukherjee D, 1980). In a response to a starred question (No. 202)
in the Indian Parliament on 8/8/2005, the Agriculture Minister revealed the following information:
Statement indicating the extent of pesticide residues in various agricultural commodities Monitored
under All India Network Project on Pesticide Residues
On Vegetables (cabbage, cauliflower, brinjal, okra, potato, beans, gourds, tomato, chilli,
Spinach, carrot, cucumber, cowpea etc.)
Year No. of Samples analysed Samples above MRL (%)
1999 277 10 (3.6%)
2000 712 81 (11%)
2001 796 93 (11.7%)
2002 592 54 (9%)
2003 666 35 (5.3%)
Total 3043 273 (8.97%)

On Fruits (apple, banana, mango, grape, orange, pomegranate, guava, chikoo, ber etc.)
1999 122 8 (6%)
2000 378 8(6%)
2001 378 0 (0%)
2002 359 3 (0.8%)
2003 317 1 (0.3%)
Total 1554 15 (0.97%)
In Milk
1999 194 116 (60%)
2000 537 94 (17.5%)
2001 468 71 (15%)
2002 No study done
2003 No study done
Total 1199 281 (23.4%)
These findings are at great variance with the results from other independent studies, which
reveal these rates to be much higher. During the Joint Parliamentary Committee probing of
the pesticide residues study reported by Centre for Science & Environment [CSE, Delhi], the
Ministry of Agriculture furnished a note to the Committee on the reasons for agricultural
Pesticide residues being high in India.
Of the 165 pesticides currently approved for use, tolerance levels have so far been included under Rule
65 of the PFA Rules for only 71 pesticides. This is less than 50% of the registered pesticides. Those not
included under the PFA Act include some pesticides termed "deemed pesticides", which were approved
prior to 1971 and for which, therefore, no data is available for undertaking risk assessment from the
point of view of food safety and for fixing Maximum Residue Limits. The agricultural sector consumes
around 67% of the pesticides produced; within the agricultural sector, two thirds of the consumption is
taken up by just a few crops like cotton, paddy, vegetables and fruits.
Pesticides consumption – India – gms / hectare:
Andhra Pradesh 302
Bihar 82
Gujarat 331
Haryana 827
Karnataka 201
Madhya Pradesh 61
Maharashtra 168
Punjab 889
Tamil Nadu 261
Uttar Pradesh 285
West Bengal 372
During evidence to the Joint Parliamentary Committee formed in 2004, a representative of
the Ministry of Agriculture and the Director General of Health Services admitted that, out of
181 pesticides registered at that time, tolerance limits (MRLs) have been fixed for only 71
pesticides. For another 50 pesticides, such tolerance limits were in the process of finalization.

It has been concluded that there are about 27 pesticides registered in the country which do not
require fixation of tolerance limits. This means 32 pesticides which are still left for tolerance
limits to be fixed; for eight of these, it was decided to follow Codex norms for the time being
since data was not available and was being collected. Data for 24 pesticides, which are
“deemed-to-be-registered” has been submitted.
Widespread usage is causing health problems due to residues of pesticides in food and pollution of
drinking water. The most worrying types of chemicals are those which are hormone disrupters and
which can build up inside the human body. Hormone disrupters interfere with our body’s hormones.
Our hormones regulate our day-to-day bodily functions and are vital for making sure we grow up
healthy. Some chemicals that we can’t break down properly will accumulate in the body’s tissues. This
is known as bioaccumulation. The risk with these chemicals is that the long-term effects of some of
them are not known and we would be unable to remove them from our bodies and environment if they
were found to be harmful. Food is major pathways to body burden. Vegetable group constitutes part of
core Indian diet.
Organophosphorus pesticides are widely used in agriculture due to their high insecticidal activity. They
are toxic organic chemicals which can irreversibly inhibit acetylcholinesterase (AChE) which is essential
for the function of the central nervous system. As the pesticide residue is a potentially serious hazard
to human health, the control and detection of pesticide residue plays a very important role in
minimising risk.
Many methods have been developed in the last few years for the detection of organophosphorus
pesticides. The most widely used methods are gas chromatography (GC), high-performance liquid
chromatography (HPLC),gas chromatography-mass spectrometry(GC-MS) ,immune assay and
fluorescence.
Chemiluminescence (CL) is defined as the production of electromagnetic radiation (ultraviolet, visible
or infrared) observed when a chemical reaction yields an electronically excited intermediate or end
product, which either luminesces or donates its energy to another molecule responsible for the
emission. The CL phenomenon can be applied as detection technique for the monitoring of a wide
variety of compounds in diverse fields, such as clinical, pharmaceutical, biomedical, environmental and
food analysis. Compared with those methods mentioned above, the Chemiluminescence(CL) method
has been growing in popularity and acceptance because of its advantages such as high sensitivity, rapid
assay speed and simple instrumentation. CL method has been applied to the determination of
organophosphorus pesticides residues during recent years.
Quinalphos (O,O-diethyl-O-quinoxalinyl phosphorothioate) is one of the most widely used
Organophosphorus insecticides in agriculture, and is applied to control of incidence of pests over crops
such as cotton, tea, citrus and rice. At present, most of the analytical methods employed for the
detection of quinalphos residues are based on chromatographic techniques, chromatographic
techniques-mass spectrometry and fluorescence.
The primary concern of the chronic low dose toxicity in man and animals is related to the carcinogenic,
teratogenic, mutagenic, immunotoxic, immunopathological and/or neuropathic effects of pesticides.
The perusal of literature in this regard reveals the studies directed towards only one or two pesticides
while in nature, when a large number of pesticides are present and their combined effect has not been
measured; which of course will give very dangerous view. Various Pathological effects of low doses of
pesticides in animals and man are as under:
1. Immunopathological effects: Immunopathological effects of pesticides in animals and man are
classified under acquired immunodeficiency or immunosuppression, autoimmunity and hypersensitivity.
They are considered to be the cause of vaccinal failures or occurrence of disease epidemics in animals
and man due to lowered immunocompetence. It has also been reported that a state of

immunosuppression for a longer period may also lead to the development of neoplasms as the immune
surveillance mechanism becomes defective. Such animals also exhibit recurrent bacterial infections
due to defective phagocytic machinery of the body. Organochlorine group of pesticides binds with
certain proteins of the body to become antigen leading to initiation of an autoimmune response in
body. Autoimmune glomerulonephritis or autoimmune hemolytic anemia or autoimmune rheumatoid
arthritis are such manifestations in animals and man. Eczema in man was found due to maneb, 2,4-D
and 2,4,5-T. DDT has also been known to cause type I hypersensitivity reaction. The dust of pesticides
is cause of allergic respiratory disorders like asthama. Cutaneous allergy has been known to occur due
to contact of pesticide contaminated food items.
2. Carcinogenic effects: Most of organochlorine pesticides like dieldrin, gamma isomer of BHC, DDT and
PCB may cause cancer in liver and lung. Indirectly, a state of immunosuppression for a longer period is
helpful in increasing the susceptibility of an animal for malignancy. Since many pesticides are known to
cause mutation in chromosomes of man and animals, it is considered that they may also lead to
carcinogenicity.
3. Mutagenicity: Pesticides may cause alterations in structure or number of chromosomes resulting in
translocations, mutations and chromosomal breakage. The altered chromosomal number may become
lethal during fetal stage. Several pesticides like DDT, Endrin, PCB and HCB are known to cause
chromosomal aberrations. The mutagenic effect of pesticide poses a more serious threat to the future
of human race.
4. Teratogenicity: The accumulation of pesticides in body tissue and congenital birth defects in
children has not been well correlated so far. However, there are certain pesticides which causes
teratogenic defects in animals. Carbaryl, thiram, propoxur, parathion, leptaphos, 2,4-D, lindane and
diazinon are having teratogenic defects in animals. In mice, cypermethrin, alphemethrin and malathian
are found to exert birth defects in baby mice.
5. Neuropathy: Most of the organophosphates, organochlorines carbamates may cause neutrotoxic
effects in man and animals including increased irritation, loss of memory, in coordination of
movement, ataxia, delayed response, convulsions, spasms and paralysis. Such changes appear due to
demyelination of nerves in central and peripheral nervous system. Pesticide residues are also
responsible for marked behavioural changes in man and animals.
6. Nephropathy: The pesticide residues present in food stuff may act as happen and when they bind
with certain body proteins, they may become antigenic. This antigenicity is responsible for initiation of
immune response in body and a continuous presence of antigen and antibodies in body may lead to the
formation of immune complexes. The immune complexes when produced in excess are deposited in
glomerular basement membrane leading to glomerulonephritis, commonly known as renal failure for
which patient needs dialysis after a regular interval to survive.
7. Hepatotoxicity: The pesticide residues in food may harm liver tissue as they are metabolised here.
There are instances of chronic liver disorders leading to cirrhosis. Certain pesticides are not so
dangerous but their metabolites cause severe damage to hepatic parenchyma. The cirrhosis once
starts; it never stops even after withdrawal of the primary cause.
8. Reproductive Disorders: It has been observed that the pesticides are lethal to dividing cells of
genitalia. They may cause abnormalities in sperms leading to decrease their ability for fertilization. On
the other hand the ova becomes defective and not able to implant on the uterine surface leading to

early abortion or miscarriage. DDT has been found to cause weak egg shell in birds leading to their
decreased population. The pesticide residues in food, thus may ultimately lead to sterility, early
abortion, still births or repeat breeding.
Adding to a growing body of literature linking persistent pesticides to diabetes, a new study in the
online journal Environmental Health Perspectives has found an increased rate of hospitalization for
diabetes in those who live close to hazardous waste sites containing persistent organic pollutants
(POPs). While established risk factors for diabetes, such as obesity, genetics and a sedentary lifestyle,
have been emphasized in prevention efforts, increasing evidence is showing exposure to environmental
contaminants is also an import risk factor that needs to be taken into account
Top Five Pesticides Found in Food
• 23% DDT (organochlorine) First used as an insecticide in 1939. Still used in India (.0001–.031 parts per
million found in the samples).
• 20% Chlorpyrifos-methyl (organophosphate) Used on stored grain since 1985. Moderately persistent in
the soil (.0001–.537 ppm).
• 18% Endosulfan (organochlorine) Introduced in 1954. Moderately persistent in the soil
(.0001–.266ppm).
• 16% Malathion (organophosphate) One of the earliest organophosphates—introduced in 1950. Low
persistence in the soil (.0007–.080 ppm).
• 15% Dieldrin (organochlorine) Second only to DDT in use between 1950 and 1970. (.0001–.020 ppm).
About 20 per cent of Indian food products contain pesticide residues above tolerance level compared to
only two per cent globally. No detectable residues are found in 49 per cent Indian food products
compared to 80 per cent globally. It is all because of following reasons which needs to be looked in
order to reduce the level of pesticide residues in animal products and other food material below MRL
value.
Reasons for more pesticide residues in India: Indiscrimate and improportionate use of pesticides:
The use of pesticides is comparatively more in certain crops while in some it is negligible. The farmers
use pesticides more frequently and in increased doses than the recommended doses or procedures. It
leads to the presence of high amount of residues in food commodities. The pesticides are used
improportionately in India in relation to places and the amount of pesticides residue varies from one
place to another.Pesticide residues in the feed and fodder are solely responsible for their accumulation
in animal and poultry. The states like Tamilnadu, AP, Punjab, Haryana, and Karnataka have highest use
of pesticides in order to get more production while on the other hand the states like Bihar, West
Bengal, North eastern states have lowest use of pesticides.
Status of pesticide residues in India: The presence of pesticide residues have been detected in
various items and in food chain. The levels of the pesticides are found much higher than expected
because of heavy contamination of environment. Besides, there are human milk, fat or tissue samples
screened for the presence of pesticide residues were also found to have very significant levels of
harmful pesticides. The BHC has been found from 0.120 to 1.22 PPM in human fat samples. Heptachlor,
an organochlorine pesticide was found to be 0.425 PPM and DDT from 0.195 to 1.695 PPM. Even human
breast milk is not free from DDT, which was found to have even 2.39 PPM levels. Similarly human blood
was found to have a much higher concentration of 12.00 PPM as against of 0.050-PPM safe levels (no
effect levels).

Main risks and target organs
Organophosphorus pesticides can be absorbed by all routes, including inhalation, ingestion, and dermal
absorption. The toxicological effects of the organophosphorus pesticides are almost entirely due to the
inhibition of acetylcholinesterase in the nervous system,resulting in respiratory, myocardial and
neuromuscular transmission impairment. A few organophosphorus pesticides have produced the so-
called "Intermediate Syndrome" and delayed neuropathy, the latter apparently unrelated to
acetylcholinesterase inhibition.
Body Burden:
The sources for body burden are everywhere -- industry, foods, and many that are not obvious. At least
75,000+ chemicals are in copious use and more than 23,000,000 are cataloged. Approximately 1,000
new chemicals are introduced each year. Scant data exists regarding the chronic (long term, low level)
health risks of most chemicals.
Scientists are generally trained to believe that "the dose makes the poison". Once a dose is low enough
not to cause an effect, it is assumed that there is no need to test even lower doses. Most chemical
safety policies are based on this premise. The lowest level tested with no effect is used as a basis to
establish safe standards for exposure to people. But new research is demonstrating that harm can
occur at much lower thresholds than previously considered possible. When smaller amounts cause
greater effects than larger amounts the effect is called hormesis. Scientists are learning that many
chemicals exhibit hormesis.
Furthermore, the timing of toxic exposure plays a much more significant role than previously
recognized. As a result, current safety standards based on high dose experiments don't guarantee
shelter from toxic levels of exposure. Health data that does exist about a chemical is usually limited to
effects when isolated from other variables. But contaminants are known to occur in complex mixtures
in the environment. A wide range of conditions are at play, and chemicals can behave very differently
when combined with other chemicals.
Harm can be amplified when chemicals are combined. Synergistic toxicity is common. Even the body's
own natural chemicals, such as hormones, can exhibit synergistic toxicity with other chemicals.
Heavy metals, organophosphates, and other chemicals damage cells by excitotoxic activity.

Excitotoxins are deliberately added to a wide range of foods. Excitotoxins increase synergistic toxicity.
Some toxins that were banned decades ago persist in the soil, air and water. They can still pass
through the skin, nostrils or mucus membranes and into the bloodstream and body tissue.
Genetic susceptibility plays a role in body burden.
Large parts of the population, possibly more than 20%, are unable to effectively excrete heavy metals.
Their burden accumulates faster. Their illnesses are more obvious. New evidence is showing that each
person has an individualized genome — a unique pattern of whole DNA sections gained or lost. Some
chemicals change genes on-the-fly. Some of these genetic changes become permanent and are passed
down in heredity.
Viruses, bacteria, yeasts, parasites, and mold aggravate body burden at any stage of life. Beyond the
better understood mechanisms of infection, research is revealing that some microorganisms interact
directly with chemicals to enhance susceptibility to infection. Each person's body burden is likely to
fluctuate over the course of hours, months, and years depending on their particular exposures and
metabolism. The science of body burden is complex and still in early stages. Nonetheless it is becoming
abundantly clear -- the spectrum of both 'rare' and 'common' illnesses is on the rise, and research is
making a connection with the mechanisms of toxic body burden.

Excitotoxins cause neurons to become so over-excited that
they burn out and die.
Neurotransmitters are chemicals that act as messengers
between cells in the brain and nervous system.
When an impulse arrives at neuron, neurotransmitter molecules are released from its axon. The
molecules diffuse across a short gap and bind with an empty receptor on the surface of another
neuron, or on a muscle or gland.
There are many different neurotransmitters and more than one kind might be used between an axon,
gap, and receptor (together called a synapse). When metabolic processes are functioning normally, the
concentration of neurotransmitter is quickly reduced and cellular 'housekeeping' takes place to keep
everything healthy and in balance. Everything happens in milliseconds or less.
Too much of a neurotransmitter makes it excitotoxic. The receptors over-activate. Ultimately the
nerve cannot keep up and kills itself (apoptosis) or triggers a nearby cell to devour it (phagocytosis).
Mitochondria are tiny structures found inside nearly every cell in the body including neurons. They
convert food molecules (like glucose) into a chemical called ATP. These ATP molecules are the energy
source for metabolic processes.
Any time a cell's energy is reduced it becomes dramatically more sensitive to glutamate. Even normal
levels of glutamate become excitotoxic when cell energy is low. Brain cells are particularly affected.
During excitotoxicity, ATP production may be reduced, stopped or even reversed. When mitochondria
malfunction, all sorts of cellular disruption and failure occur. Numerous examples can be found starting
here, here, and here. Genetic mutation is associated with excitotoxicity and mitochondrial
malfunction.

Excitotoxicity also causes high levels of calcium (Ca2+ ions) to enter cells, in
turn activating a variety of enzymes which proceed to damage cell structures including DNA. (For a
deeper look at the role of calcium channels look here.)
Altogether, the human cell nucleus is currently estimated to encode between 250,000 and 1,000,000
proteins (of which only a fraction have been identified). Mitochondria have their own DNA entirely
separate from DNA in the cell nucleus. The mitochondrial genome is ~ 16,000 genetic 'letters' compared
with ~ 3,000,000,000 in the nuclear genome. Mitochondrial DNA encodes 13 proteins, but mitochondria
also use ~ 1,500 proteins encoded by the cell nucleus.
Plus, the role of RNA in excitotoxicity is just begining to emerge. The vast number of possible genetic
mutations and protein deviations -- and the extensive cascade of symptoms that ensue -- help explain
why excitotoxicity is fundamental to so many diseases.
Illnesses commonly labeled as 'mysterious' are being traced back to excitotoxicity. This list of diseases
helps convey the wide array of conditions consistent with excitotoxic mechanisms. Excitotoxins
promote cancer growth and metastasis. Cancer cells become more mobile when exposed to aspartate
or glutamate. Exposing a tumor to glutamate has been compared with giving it fertilizer -- it grows like
wildfire. It can make a curable cancer incurable. Stem cells subjected to excitotoxicity may turn out to
play a vital role in the formation of cancers and other diseases.
Glutamate is the most abundant neurotransmitter in the brain. Glutamate receptors also exist in every
part of the body. They are found throughout the heart, the digestive system, and in every vital organ.
Aspartate is a neurotransmitter found abundantly in the spinal cord. Glutamate and aspartate are
excitatory neurotransmitters (as opposed to GABA and glycine which are inhibitory neurotransmitters).
Glutamate comes from glutamic acid and aspartate comes from aspartic acid. Glutamic acid and
aspartic acid are "non-essential" amino acids. The body synthesizes just the amounts needed via a
tightly regulated metabolic process.
In unprocessed whole foods, glutamic acid and aspartic acid are not free amino acids. They are bound
together with other amino acids in complex proteins. They get digested and absorbed as combined
amino acids. They get broken down in the liver and released at very low levels the body can deal with.
Excess glutamic acid or aspartic acid is detrimental and results in excitotoxicity.
Hydrolysis is a process in which proteins and starches are broken down into amino acids, simple sugars,
and fatty acids. Hydrolysis can be achieved using chemicals, enzymes, heat, and other techniques.
Except in rare cases, two particular amino acids are always liberated in the process -- Asparagine (Asn)
and Glutamine (Gln). These convert to aspartic acid and glutamic acid. Processed foods are a
significant source of excitotoxins.
A chief reason excitotoxins are used is to make food 'taste better'. The two most familiar examples are

aspartame and MSG, but there are many others. It's worth reading here to see how hydrolysis affects a
seemingly innocuous ingredient like "partially hydrolyzed guar gum".
Food labels offer few clues about excitotoxic ingredients. Sometimes an excitotoxin is not explicitly
listed, but cohorts are. For example, disodium inosinate (E631) and disodium guanylate (E627) are food
additives often found in instant noodles, potato chips, and a variety of other snacks. They are used as a
flavor enhancers in synergy with monosodium glutamate. They are relatively expensive additives and
are not used independently of glutamic acid; if disodium inosinate or disodium guanylate are present in
a list of ingredients but MSG does not appear to be, it is likely that glutamic acid is hidden inside
another ingredient.
Soybeans are naturally high in glutamic acid. When soy extracts are produced (hydrolysis) the glutamic
acid is released and concentrated. The resulting levels are often higher than in MSG-labeled products.
Batches of yeast are broken down to provide amino acids -- on a food label this may be read as 'yeast
extract'. These are also a source of highly concentrated excitotoxins.
Citric acid is most often made from the fermentation of corn sugars. Free glutamic acid is introduced
from the protein remnants hydrolyzed during production. Be aware too that citric acid is often
produced at chlor-alkali facilities, and mercury contamination may have occurred early in the process.
Excitotoxins penetrate the placental barrier and reach the fetus. Some consequences are
• Cumulative harmful effects on the endocrine and reproductive systems
• Changes in the brain that are irreversible, particularly the hypothalamus
• Deterioration of the nervous system, organs and tissues
Infant formulas are typically based on soy. Many baby foods contain ingredients like 'caseinate
hydrolyzed protein broth' which is a significant source of glutamate. Excess glutamate impairs a baby's
nervous system and can contribute to developmental delays. It can lead to juvenile obesity. It can lead
to sudden infant death (SIDS). Most restaurants don't actually know whether they are serving
excitotoxins. Most chefs and cooks don't know about the large list of excitotoxins to look out for. They
can claim "no MSG added" but not realize excitotoxins are in bulk ingredients that arrived without much
labeling. Snack foods, soft drinks, fast foods -- all are loaded with excitotoxins. Most sports drinks,
energy bars, and protein powders are also loaded. 'Edible' films and coatings applied to foods -- both
fresh and processed -- have various formulations that include hydrolyzed proteins. Produce that has
been 'waxed for appeal' can contain excitotoxin in the wax.
Glutamate receptors exist in all organs and tissues. Consuming a meal or drink containing MSG can
elevate glutamate in the blood by 20x. When the glutamate receptors over-stimulate in response,
effects such as these can be experienced :
• Brain — headaches (including migraines), irritability, aggression, depression, confusion,
uncontrollable cravings, seizures
• Esophagus — reflux, indigestion
• Bowel — irritable bowel, diarrhea

• Nerves — tingling sensations, ringing in the ears, visual sensitivity, changed sense of taste or
smell
• Heart — cardiac arrhythmia and cardio artery spasm (heart attacks, both can be fatal)
There are glutamate receptors on both sides of the blood brain barrier.
Exposing these receptors to excess glutamate causes irregular opening of the barrier. This compromise
in the brain's defense system allows chemicals, viruses, bacteria, and other foreign substances to move
in. A similar problem can occur in the intestines. Normally, cells regulate the molecules allowed to
pass through, and structures called "tight junctures" seal the gap between intestinal cells so that
molecules don't sneak by.
Excitotoxicity can cause these tight junctures to open up and allow molecules through. Technically this
is known as "paracellular transport" but more commonly it is known as "leaky gut". Other tissues — such
as bladder and kidney — can be leaky like this too. Excess neurotransmitters aren't the only chemicals
that contribute to excitotoxicity. Others include
• Chemicals capable of binding with receptors, or otherwise eliciting a reaction at receptors --
essentially stealing seats and hanging around
• Chemicals that interfere with enzymes responsible for naturally reducing neurotransmitter levels --
insecticides and nerve agents (chemical warfare) are examples
• Chemicals that interfere with metabolic 'housekeeping' processes
This turns out to be a large and growing list of chemical ingredients found in pesticides,
pharmaceuticals, over-the-counter medicines, vaccines, and other products. Interestingly, many
chemicals that are excitotoxic at one level are endocrine disruptors at another.
"A number of studies have shown that mercury, in submicromolar concentrations, interferes with the
removal of glutamate from the extracellular space, where it causes excitotoxicity. This removal system
is very important, not only in protecting the brain but also in preventing abnormal alterations in brain
formation." Chemical body burden leads to increased brain immune activity that activates
excitotoxicity. Oxidative stress also promotes excitotoxic degeneration of synapses and death of
neurons.
In fact oxidative stress, excitotoxicity, and ischemia (lack of oxygenated blood flow) appear to work
together in a kind of "death spiral". This research points out that the "range of toxicants reported to
alter oxidative status is very broad" and cites a few including

• Metals such as mercury, lead, tin, cadmium, and arsenic
• Ethanol
• Herbicides such as paraquat, pyrethroids, and organophosphate and carbamate inhibitors of
cholinesterase
The ability to oxidize cells is shared by many toxicants.
Viruses can cause excitotoxicity.
Many types of virus have an affinity for nervous system tissue. When a viral infection breaches the
blood-brain barrier, it leads to inflammation within the brain -- particularly in the microglia, which
form part of the immune system of the brain. This is important because of the role of glial cells in the
brain. Astroglia cells (aka astrocytes) surround neurons and perform many functions including
• Formation of the blood-brain barrier
• Providing nutrients to nerve tissue
• A leading role in the repair and scarring process in the brain
Another very important role is to maintain a balance in the brain between excitatory and inhibitory
neurotransmitters. When the virus -- or an antibody triggered by it -- starts killing the brain’s
astrocytes, then glutamate builds up in excess. Excess glutamate is excitotoxic.
You've seen that excitotoxicity can play multiple roles in
disease progression. Yet another is by disrupting methylation. DNA methylation is involved with gene
expression. Changes in methylation can alter protein activity which can result in an array of
detrimental conditions.
This study found that Aspartame (Nutrasweet) has an effect on gene expression even after just one
week at the maximum recommended daily amount. Organs known to experience high cancer
proliferation rates were especially affected -- such as in the lymph system, bone marrow, and kidneys.
What is a "body burden"?
A: Toxic chemicals, both naturally occurring and man-made, often get into the
human body. We may inhale them, swallow them in contaminated food or water, or
in some cases, absorb them through skin. A woman who is pregnant may pass them
to her developing fetus through the placenta. The term " body burden " refers to

the total amount of these chemicals that are present in the human body at a given point in time.
Sometimes it is also useful to consider the body burden of a specific, single chemical, like, for
example, lead, mercury, or dioxin.
Some chemicals or their breakdown products (metabolites) lodge in our bodies for only a short while
before being excreted, but continuous exposure to such chemicals can create a "persistent" body
burden. Arsenic, for example, is mostly excreted within 72 hours of exposure. Other chemicals,
however, are not readily excreted and can remain for years in our blood, adipose (fat) tissue, semen,
muscle, bone, brain tissue, or other organs. Chlorinated pesticides, such as DDT, can remain in the
body for 50 years. Whether chemicals are quickly passing through or are stored in our bodies, body
burden testing can reveal to us an individual's unique chemical load and can highlight the kinds of
chemicals we are exposed to as we live out each day of our lives. Of the approximately 80,000
chemicals that are used in the United States, we do not know how many can become a part of our
chemical body burden, but we do know that several hundred of these chemicals have been measured in
people's bodies around the world.
Q: Do all humans carry this chemical body burden?
A: Scientists estimate that everyone alive today carries within her or his body at least 700
contaminants, most of which have not been well studied (Onstot and others). This is true whether we
live in a rural or isolated area, in the middle of a large city, or near an industrialized area. Because
many chemicals have the ability to attach to dust particles and/or catch air and water currents and
travel far from where they are produced or used, the globe is bathed in a chemical soup. Our bodies
have no alternative but to absorb these chemicals and sometimes store them for long periods of time.
Whether we live in Samoa or San Diego, Juneau, or Johannesburg, all our bodies are receptacles for a
multitude of industrial chemicals. Wherever we live, we all live in a chemically contaminated
neighborhood.
Some of the chemicals residing in our bodies are pesticides, and some
are used in or produced by other forms of industrial production. Many
are found in a wide variety of consumer products. Some chemicals like
dioxins and furans are created unintentionally by industrial processes
using chlorine and from the manufacture and incineration of certain
plastics. Scientists estimate that there are many other unintentionally
created by-products which have not yet been "discovered" since no
tests have yet been developed that would fully identify or describe
these by-products.
Q: How did this happen? How have I been exposed?
A: Humans are exposed to chemicals through the food we eat, the air we breathe, and the water we
drink and bathe in. Chemicals often coat the surface of dust particles, which we handle or inhale.
Contaminated dust is an especially important route of exposure for children who commonly put their
hands into their mouths. We are also exposed to hundreds of chemicals in everyday products we use.
Paints and varnishes, gasoline, glues, cosmetics, clothes dry-cleaned with solvents, plastic food
containers, and home and garden pesticides are just a few examples. The chemical landscape created
as a result of intensive and continuing chemical use during the 20th century has been internalized.
Because the chemicals found within our bodies are not labeled with return addresses, it is difficult to
identify where they come from.
For example almost all of the dioxin found inside your body got there from eating contaminated food.
However, it may have originated in a local medical waste incinerator or it may have been created by a
distant, chlorine-based, paper manufacturing plant located thousands of miles from your home.
Whatever its source, somewhere it entered the food chain and made its way into the food you ate.
Similarly, a pesticide found inside your body may have come from pesticide spraying done at a local

school, in your garden or kitchen, or it may have arrived on foodstuffs grown with pesticides. Its origin
will be difficult to identify.
Another source of exposure is the chemical body burden of our mothers.
During pregnancy, the chemicals stored in a woman's body have the ability
to cross the placenta where they may cause harm. Some chemicals from a
mother's body are also mobilized and transferred to the breasts as she
produces breast milk. These chemicals are then transferred to the baby
during breastfeeding. Breast milk remains the best food for babies, as
recent studies show, because of its immunological, nutritional and
psychological benefits. The fact that industrial chemicals have contaminated
breast milk is tragic. Ironically, breastfeeding appears to offset some of the
damage created by contaminants during fetal development. Some of the
chemicals we receive from our mothers in utero and through breastfeeding
remain with us for years, an unintended legacy that our mothers pass on as
their body burdens become our own.
Q: What is the evidence for body burden? How long have we known about this problem?
A: It has been known for centuries that chemicals can enter the body and cause health effects. Since
the middle of the 20th century, scientists have been able to detect and measure chemicals in wildlife
and humans and sometimes link these chemicals to health outcomes. For example, in 1944 researchers
found residues of DDT in human fat, and in the early 50's, naturalists rightly concluded that DDT was
directly responsible for thinning eggshells and declining populations of bald eagles and other birds. In
fact, at about the same time, DDT was detected in Antarctic penguins living an extremely long distance
from where DDT was being used.
Since then, analytic techniques have improved and many other chemicals have been detected in human
and wildlife tissues. For decades, tests for some substances that make up the total chemical body
burden have been conducted by government agencies around the world. These hundreds of studies
include analyses of adipose (fat) tissue, breast milk, semen, blood, or urine for chemical content,
documenting the amount and kinds of chemicals found
Q: What are the health effects of this body burden?
A: Chemicals can have different effects in people or in wildlife, depending on the amount, timing,
duration, and pattern of exposure as well as the properties of the specific chemical. Chemicals can
have toxic effects through a variety of mechanisms.
Chemicals that cause cancer are called carcinogens. Chemicals that cause birth defects are called
teratogens. Chemicals that damage the normal development of the fetus, infant, or child, or damage
our reproductive tissues are called developmental/reproductive toxicants. Some chemicals can
cause damage through their ability to interfere with normal hormone function. These chemicals are
called endocrine disrupters.
Through these various mechanisms, toxic chemicals can cause a long list of health problems. They
include, for example, direct damage to the lungs, liver, kidney, bones, blood, brain and other nerves,
and the reproductive systems. There are hundreds of adverse health effects that can arise from
exposures to chemicals or metals. These potential effects include cancer; high blood pressure; asthma;
deficits in attention, memory, learning, and IQ; Parkinson's-like diseases; infertility; shortened
lactation; endometriosis; genital malformation; peripheral nerve damage; and dysfunctional immune
systems. For example, dioxin is a carcinogen and fetal exposures to dioxin interfere with normal
development, including the immune system. Fetal exposure to polychlorinated biphenyls (PCBs) is
related to behavioral and cognition problems. DDT exposure has been related to women's inability to

produce sufficient breast milk. The immune systems of children in some areas of the far north are
unable to produce enough antibodies to make vaccinations effective. Since these children and their
mothers carry large chemical body burdens, a chemical link to this problem is likely. Fetal exposure to
mercury causes attention, memory, and learning problems later in life. Brain development is also
impaired in fetuses and infants exposed to lead.
Q: Are there special health effects for children?
A: Developing or immature tissues are far more susceptible to chemical exposures
than adult tissues. Development is a time of special vulnerability. It is a time of
very rapid replication and differentiation of cells - the latter being an incredibly
complex and vulnerable process.
This means that the developing fetus, infant, or child may suffer harmful impacts
from relatively small exposures that have no measurable impacts on adults. So,
for example, fetal exposures to chemicals in amounts that are safe for adults may
result in birth defects or abnormal brain development. For this reason, it is not
only the amount of the exposure that is important, but the timing of the
exposure. Unfortunately, few of the chemicals to which we are regularly exposed
to have undergone sufficient testing to fully understand whether or not they
might be harmful to a fetus or child.
Hormones play extremely important roles as they help to direct the development
of the fetus, infant, and child. Of course, hormones are also important in adults,
as they are crucial for normal functioning of many bodily systems. What is amazing about hormones is
that they are present and active in only tiny amounts, yet these tiny amounts produce major, major
effects. Most importantly, exposure to an endocrine disrupter at a low level during a critical time in
development can have lifelong impacts. For example, the developing fetus may mistake a foreign
chemical for a hormone, and this may, in turn, cause an incorrect "signal" to be sent to developing
tissues. These early mistakes can permanently damage the baby's developing immune, reproductive or
nervous systems. Most of the confirmed evidence of the importance of endocrine disrupters comes
from wildlife studies, but more recently, evidence for impacts in humans has also emerged.
Q: Can the links between body burden and illness be proven?
A: Of the more than 80,000 chemicals in commerce, only a small percentage of them have ever been
screened for even one potential health effect, such as cancer, reproductive toxicity, developmental
toxicity, or impacts on the immune system. Among the approximately 15,000 tested, few have been
studied enough to correctly estimate potential risks from exposure. Even when testing is done, each
chemical is tested individually rather than in the combinations that one is exposed to in the real world.
In reality, no one is ever exposed to a single chemical, but to a chemical soup, the ingredients of which
may interact to cause unpredictable health effects.
The good news is that in several cases, public interventions have resulted in primary prevention, the
lowering of the public's exposure, and the lowering of body burdens. For example, the removal of lead
from gasoline and the elimination of lead from most kinds of paint have resulted in a marked decline in
the lead body burden of the general population. Since lead causes lowered IQ in exposed children, this
reduction in body burdens is a hopeful sign.
The bad news is that there are still groups of children who remain at significant risk
from impaired brain function because of elevated lead levels. Many of them live in
urban environments where they are exposed to lead from numerous sources,
including leaded paint in houses, old industrial facilities, and contaminated soil. For
PCBs, current background levels cause neurodevelopmental deficits in children.

Q: How do I find out about my own body burden?
A: In general, there is no readily accessible way to know. Even if you could learn about your own body
burden, you may not find the information useful. Your doctor in general cannot prescribe treatments
that will lower the level of chemicals in your body. Finding out about your community body burden,
however, is useful, and can lead you and your neighbors to take actions to lower your chemical
exposures. Government agencies, health care facilities, or other laboratories do
not routinely offer body burden measurements. Most of what we know about
body burdens of contaminants comes from limited studies of a few
contaminants, conducted by government agencies on selected groups of
people. These studies often break down the analysis by sex, age, and race,
which provides useful information about population-wide averages. But
population-wide averages cannot predict body burdens for individual people.
Moreover, these population studies are usually limited to just a few of the
contaminants to which people are regularly exposed.
Body burden monitoring gives them a report card on their primary prevention activities. Body
burden monitoring also can serve as an early warning system that identifies new chemicals that
are increasing in people, and that the government should pay attention to.
Since we have the right to know about what chemicals are in our air, water, soil, food
and products we use daily, it makes sense that we should have the right to know about
the chemicals we carry in our bodies.
Q: What does a body burden test tell me about my own health?
A: Body burden testing tells us something about what chemicals we have been exposed to. It usually
tells us almost nothing about whether those exposures are responsible for any health problems.
However a single body burden test, or, better yet, community-based monitoring, may indicate a great
deal about the overall state of our environment and public health.
Q: How can I get these chemicals out of my body?
A: At this time there is no general agreement about useful or safe methods for reducing body burdens.
The best course is long-term prevention. Contamination of future generations by toxic chemicals can
be prevented by working together to: 1) eliminate the most dangerous persistent chemicals that
bioaccumulate (concentrate more as they get higher in the food chain); 2) develop alternative
production methods that use non-toxic materials, and 3) ensure that communities, national
governments and international agencies take a precautionary approach when it comes to chemicals
released into our air, water, and soil. Changes in lifestyles may prevent some exposures. Recent
studies of chemical body burdens in the state of Washington have found that children who ate organic
food and who were not exposed to pesticides in their homes had significantly lower body burdens.
Some limited research shows that body burdens of some contaminants stored in fat can be lowered by
a combination of special diets, exercise, and saunas. But data are very limited and preliminary. When
some metals, like lead or mercury, are present in the body at fairly high levels, "chelating agents" are
sometimes used to lower the total body burden of that particular metal. However, "chelation"
treatments are somewhat controversial with potential side effects and have not been proven to
consistently reduce toxic impacts of exposure. For example, one study showed that a chelating agent
used in children with moderately elevated lead levels did not improve neuralgic performance.
Different chemicals require different types of monitoring. Body burden monitoring is the measurement
of chemicals in our bodies. Scientific techniques now allow us to detect very small amounts of

chemicals in blood, breast milk, urine, hair, fat and other body tissues. Which of these body burden
tests to use depends on the type of chemicals being monitored. Persistent chemicals are best tested in
blood, adipose tissue (fat) or breast milk. Chemicals that pass through the body more quickly can be
found using blood or urine tests.
Similarly, environmental testing measures chemicals in air, water and soil. Food can also be tested as
an indicator of environmental contamination. For example, mercury-contaminated water can lead to
elevated levels of this metal in certain seafoods. Also, certain chemicals from industrial practices are
carried in air and can make their way into our meat, poultry and dairy supplies by being deposited on
soil or vegetation where they are then eaten by animals.
Body burden monitoring, for example, may confirm the presence of a particular chemical in a person's
system, but this information will not, with rare exceptions for a few chemicals, provide an explanation
for symptoms or an illness. Many symptoms or illnesses have many different possible contributing
factors, and it is rare for a detected chemical to be positively identified as the cause of a person's
illness. Moreover, we don't know what the vast majority of commercial chemicals do to humans
because of the lack of scientific research on the health effects of these chemicals.
It should be noted that body burden monitoring may leave individuals anxious because of the
uncertainty about whether their chemical body burden will cause future disease. It is important to
note the feeling of helplessness that some tested individuals may feel knowing that there are no
generally accepted safe and effective methods for eliminating many contaminants from their bodies.
Today, children are exposed to thousands of substances in the environment, most of which have never
been tested for toxicity to children. Lead is perhaps the best-studied of the environmental threats to
children, but there may be countless more that have never been studied. There is strong and growing
evidence that exposure to toxic chemicals in the environment contributes to many diseases of children,
among them asthma, learning disabilities, certain birth defects and childhood cancer.
Studies have been conducted on the variability and utility of whole blood and plasma organochlorine
pesticide concentration measurements in man. Concentrations of p,p′-DDE, dieldrin, and β-
hexachlorocyclohexane are remarkably consistent throughout the day. Minor increases in p,p′-DDE and
p,p′-DDT serum concentrations were observed promptly following the ingestion of the evening meal.
Apparently, concentrations of organochlorine pesticides in the blood are in equilibrium with those in
the tissue and measurement constitutes a highly useful and readily obtainable means of estimating
body burdens and exposure. Many of the pesticides found in the test subjects have been linked to
serious short- and long-term health effects including infertility, birth defects and childhood and adult
cancers. Chemical Trespass finds that children, women and Mexican Americans shoulder the heaviest
“pesticide body burden.” For example, children—the population most vulnerable to pesticides—are
exposed to the highest levels of nerve-damaging organophosphorous (OP) pesticides.
The report introduces the Pesticide Trespass Index (PTI), a new tool for quantifying responsibility of
individual pesticide manufacturers for their “pesticide trespass.”
Q: What are organochlorine pesticides?
A: Organochlorine pesticides are insecticides composed primarily of carbon, hydrogen, and chlorine.
They break down slowly and can remain in the environment long after application and in organisms
long after exposure.

The most notorious organochlorine is the insecticide DDT (Dichloro diphenyl trichloroethane). Promoted
as a "cure all" insecticide in the 1940s, DDT was widely used in agricultural production around the world
for many years. It was also the chemical of choice for mosquito control; until the 1960s, trucks sprayed
DDT in neighborhoods across the U.S. DDT was also the primary weapon in the global "war against
malaria" during this period, and continues to be used for malaria control in a handful of countries.
Q: How are organochlorines used?
A: Organochlorine pesticides are mostly used as insecticides. Specific uses take a wide range of forms,
from pellet application in field crops to sprays for seed coating and grain storage. Some
organochlorines are applied to surfaces to kill insects that land there. An example of this strategy is
the spraying of interior home walls with DDT to control mosquitos and the malaria they carry. This is
the way DDT is usually applied in those countries that are still using the pesticide for malaria control.
Other organochlorines - such as chlordane, heptachlor and pentachlorophenol - are used to treat wood
to prevent pest damage.
Some organochlorine pesticides are used on a wide array of crops. Endosulfan, for example, was first
registered as an insecticide and miticide in the U.S. in 1954. It is still in widespread use in the U.S. to
control pests in vegetables, fruits, cereal grains, and cotton, as well as ornamental shrubs, trees,
vines, and ornamental plants. Internationally, its use in African cotton production is common, and it is
applied to control pests on cashew plantations in India.
Lindane is another organochlorine with a range of uses. lindane has been used to protect crop seeds
from insects, for pest control in forests, on livestock and household pets for control of ticks and other
pests, and in homes to control ants and other household pests. It is also the active ingredient in many
medicated shampoos and soaps to control head lice and scabies. Lindane is now restricted to
seedcoating uses for a handful of grain crops, and continues to be used to control lice and scabies.
Internationally, lindane is banned or severely restricted in 40 countries.
Q: Are organochlorines in our bodies? How do they get there?
A: Yes. Organochlorines are some of the chemicals found most often in the hundreds of tests of human
body tissue - blood, adipose tissue, breastmilk - that have been conducted around the world. Because
of their chemical structure, organochlorines break down slowly, build up in fatty tissues, and remain in
our bodies for a long time.
Pesticide residues on food are a major source of organochlorine exposure. In a recent analysis of
organochlorine residues in the U.S. food supply, Pesticide Action Network found that even those
chemicals that have been banned for decades are showing up consistently in food samples tested by
the U.S. Food and Drug Administration. This can be explained in part by the long life of many
organochlorines in the environment (dieldrin and the breakdown products of DDT, for example, can
remain in soil for decades), and in part from the transport on wind and water currents - as well as food
imports - of pesticides that continue to be used in other countries.
Q: How do organochlorines affect our health?
A: Organochlorines contribute to many acute and chronic illnesses. Symptoms of acute poisoning can
include tremors, headache, dermal irritation, respiratory problems, dizziness, nausea, and seizures.
Organochlorines are also associated with many chronic diseases. Studies have found a correlation
between organochlorine exposure and various types of cancer, neurological damage (several
organochlorines are known neurotoxins), Parkinson's disease, birth defects, respiratory illness, and
abnormal immune system function. Many organochlorines are known or suspected hormone disruptors,

and recent studies show that extremely low levels of exposure in the womb can cause irreversible
damage to the reproductive and immune systems of the developing fetus.
Q: How is the government regulating organochlorines?
A: Many organochlorines have been banned in the U.S. and other countries because of concerns about
environmental impacts and human health effects.
In addition to DDT, the United States has banned aldrin, dieldrin, arochlor, chlordane, heptachlor,
mirex hexachlorobenzene, oxychlordane, toxaphene and others. However, several organochlorines are
still registered for use, including lindane, endosulfan, methoxychlor, dicofol and pentachlorophenol.
Some organochlorines have been targeted for global elimination under the recently signed Stockholm
Convention on Persistent Organic Pollutants (POPs). The treaty is an international effort to phase out
harmful chemicals that persist in the environment and can be transported around the world. Many
organochlorines fall into this category. The initial list of 12 chemicals targeted by the treaty includes
nine organochlorine pesticides.
Organophosphorus pesticides
The OP pesticides work by interfering with the nervous system of insects, a mechanism that also
affects the human nervous system when people are exposed. Other health effects of individual OP
pesticides vary; some are highly acutely toxic, some cause development or reproductive harm, and
some are known or suspected endocrine disruptors.
Q: What are organophosphorus pesticides? How are they used?
A: As many of the first-generation organochlorine pesticides were banned in the 1970s, the
agrochemical industry turned to the less persistent, but more acutely toxic organophosphate (OP) and
carbamate compounds to control insect pests. Use of these pesticides increased rapidly, and by the
late 1980s about 65% of insecticides applied nationwide were OPs and (closely related) carbamate
compounds. Use has increased slightly since then to about 70% of total insecticide use.
Q: Do we know organophosphorus compounds are in our bodies? How do they get there?
A: Widespread exposure to the OP pesticides has recently been documented through research done by
the CDC and academic scientists, which show that most people have breakdown products of these
pesticides in their urine. Because OP pesticides generally do not persist in the environment for long
periods of time and do not build up in the body fat of humans and other animals, the fact that these
pesticides were found in such a high percentage of test subjects indicates that most people are
routinely exposed to these chemicals on a daily basis.
People are commonly exposed to OP pesticides through eating fresh and processed vegetables,
contacting pesticide-contaminated surfaces, breathing air near pesticide applications (both indoors and
outdoors), and drinking pesticide-contaminated water. The multiple uses and ubiquitous nature of
these chemicals result in routine exposures to many different OP pesticides for most people.
Q: How do organophosphorus pesticides affect our health?
A: Organophosphorus compounds block production of an enzyme called cholinesterase (ChE), which
ensures that the chemical signal that causes a nerve impulse is halted at the appropriate time. OPs are
among the most acutely toxic pesticides, some OP pesticides cause developmental or reproductive
harm, some are carcinogenic, and some are known or suspected endocrine disruptors.

Phthalates are a class of chemicals commonly used in consumer products. Phthalates cause a wide
range of adverse health problems including liver, kidney and lung damage as well as reproductive
system and sexual developmental abnormalities. Phthalates are classified as “probable human
carcinogens.”
Q: What are phthalates and how are they used?
A: Phthalates are a class of chemicals added to a number of common consumer products. In 1994,
close to 87% of all phthalates in the United States were used as plasticizers, or softening agents, in
vinyl products. Plasticizers are molasses-like materials that saturate a three-dimensional matrix, such
as a stiff sponge. Beyond vinyl, humans are further exposed to phthalates in cosmetics and scented
products such as perfumes, soaps, lotions and shampoos. Phthalates are also added to insecticides,
adhesives, sealants and car-care products.
Q: Do we know phthalates are in our bodies? How do they get there?
A: A study released by the CDC in 2001 confirmed that humans have certain phthalates in our bodies.
Eating, breathing and skin contact, as well as blood transfusion, are all ways, either together or alone,
that phthalates make their way into our bodies. According to the U.S. Environmental Protection
Agency (EPA), eating is probably the main route by which humans are contaminated with diethylhexyl
phthalate (DEHP), the most widely used phthalate plasticizer. DEHP migrates into food from certain
foodwraps during storage. Similarly, we are also contaminated with other commonly used phthalates
such as diisononyl phthalate (DINP).
Children may take in higher than average amounts because many chew toys are made
of highly phthalate-softened vinyl (for example, teethers). Indeed, the highest levels
of DINP released from teethers and toys exceeded the acceptable daily intake level in
studies, conducted in the Netherlands and Denmark, that simulated children's
mouthing behavior. Furthermore, a Dutch study confirmed what most of us have
observed --- children suck or chew their fingers and other things that are not intended to go into their
mouths more than chew toys. This instinctive chewing undoubtedly adds to their overall intake of
phthalates.
Blood transfusion is another route of human phthalate intake. Phthalates make their way from vinyl or
PVC medical devices into solutions that are then fed into the patient. People who are ill, especially
children whose systems are still developing, may be particularly sensitive to this type of exposure. The
American Medical Association (AMA) voiced concerns about DEHP-containing medical devices, and a
Health Canada Advisory Panel further recommended that health care providers not use DEHP-
containing medical products in certain patient groups including infants and males before puberty.
Concerns have in fact been raised by the National Toxicology Program that the developing, but not
mature, male genital tract in humans may be adversely affected by high levels of DEHP.
Breathing in air and dust containing phthalates that have escaped from vinyl flooring also adds to the
amount of phthalates in our systems. Again, this is particularly worrisome for children since they spend
a lot of time indoors breathing close to the floor. In fact, an initial study conducted in Norway
reported a higher incidence of bronchial obstruction in children living in houses with vinyl, as opposed
to wooden, floors. Phthalates being released into the air may be the link between these two
observations.
Skin contact could be a very important route of phthalate intake from personal care products such as
soap. In the CDC study of phthalates, the breakdown product of diethyl phthalate (DEP) was detected
in the highest level in the tested population. DEP is used in a number of scented products such as
soaps, lotions and perfumes. DEP is also found in plastic products like toothbrushes, toys and food
packaging.

Q: How do phthalates affect our health?
A: Recently, the National Toxicology Program (NTP) expressed concern over the adverse development
of babies born to pregnant women who take in DEHP at the normal levels estimated for an adult. They
also expressed concern that male infants and toddlers who substantially exceed adult DEHP intake
estimates could suffer problems in their reproductive system development.
Rats and mice fed DEHP and DINP also showed an increase in liver cancers over animals that had not
been fed the chemicals. High doses of diethyl phthalate (DEP) given to female rats have been shown to
cause the growth of an extra rib in their offspring. Additionally, female animals exposed to DEP
throughout their lives experience an elevated number of stillbirths.
Q: How is the government regulating phthalates?
A: In 1999, prompted by the potential of babies to intake dangerous amounts of phthalates and the
serious, negative health effects found in animal studies, the European Union placed an emergency ban
on the use of certain phthalates in toys made for children under the age of three. This emergency ban
was recently renewed. In the United States, the Consumer Product Safety Commission (CPSC) and the
Toy Manufacturers of America (TMA) agreed upon a voluntary limit of DEHP at 3% in pacifiers and
teethers in 1986. Later in 1998, the CPSC asked toy manufacturers to voluntarily withdraw vinyl
teething rings and rattles containing the phthalate DINP from the market. However, such voluntary
agreements do not stop the use of, and children’s exposure to, hazardous or untested additives.
Similarly, adults are also exposed to potentially hazardous chemicals by using any number of phthalate-
containing products.
Dioxin is one of the most studied chemicals on the planet. It is found
throughout the environment and in our food supply. It causes a wide range
of adverse health effects including cancer, birth defects, diabetes,
learning and developmental delays, endometriosis, and immune system
abnormalities. It is the most potent animal carcinogen ever tested.
Q: What is dioxin and how is it created?
A: Dioxin is a family of chemicals containing carbon, hydrogen and chlorine. There are seventy-five
different forms of dioxin, with the most toxic being 2,3,7,8-tetrachlorodibenzo-p-dioxin or TCDD.
Dioxin is not deliberately manufactured. Rather, it is the unintended by-product of industrial
processes that use or burn chlorine in the presence of organic materials.Top three sources of dioxin are
municipal waste and hospital incinerators and backyard burn barrels. Additional sources include
chemical processing facilities that use chlorine to make products such as polyvinyl chloride (PVC)
plastic and pesticides and pulp mills that use chlorine to bleach wood pulp to make paper white.
Q: Do we know dioxins are in our bodies? How do they get there?
A: There is little or no "margin of exposure," meaning that we are nearly "full" and that any additional
exposure of dioxin can result in adverse health effects. Some people already have body burden levels
that are above average and they may already be suffering adverse health effects.
Q: How do dioxins affect our health?

A: Exposure to dioxin can lead to a wide array of adverse health effects including cancer, birth
defects, diabetes, learning and developmental delays, endometriosis, and immune system
abnormalities. Dioxin is a known carcinogen. IARC, the International Agency for Research on Cancer,
which is part of the World Health Organization, classified it as a known human carcinogen in 1997. In
January 2001, the Department of Health and Human Services' National Toxicology Program classified
dioxin as a known human carcinogen. The September 2000 draft of the U.S. EPA's Health Assessment
document on dioxin also classifies dioxin as a known human carcinogen. Dioxin also causes a wide range
of non-cancer effects including reproductive, developmental, immunological, and endocrine effects in
both animals and humans.
Q: How is the government regulating dioxins?
A: Despite the alarming information about the dangers of dioxin, the Chlorine Chemistry Council has
launched an attack to gut any efforts to eliminate dioxin or adopt a precautionary approach.
The Stockholm Convention on Persistent Organic Pollutants is an international treaty aimed at
eliminating a dozen harmful chemicals including dioxins and furans. The convention was signed in May
2001 and will be valid after it is ratified by 50 countries. While the Bush Administration signed the
Stockholm Convention in May 2001, the U.S. has not yet ratified the treaty.
Women's physiology and role in society make them bear the brunt of environmental toxins. There has
been an alarming rise in endometriosis and cancers amongst women worldwide. A major source of the
problem could literally be in the air. Excruciating pain during menstruation; excessive bleeding; painful
intercourse; infertility and bowel problems are a daily reality for women living with endometriosis, a
puzzling disease in which the tissue of the endometrium (uterine lining) of some women is found
outside the uterus – on the ovaries, intestines, bowels. This tissue responds to cyclical hormonal
stimulation, bleeds and build up into nodules and cysts. W omen with endometriosis have a higher rate
of allergies, asthma and chemical sensitivities and are also at higher risk for autoimmune diseases and
certain cancers. Yet, this debilitating disease affecting an estimated 89 million women and girls around
the world is still comparatively unheard of.
Several environmental pollutants including pesticides like DDT, PCBs and dioxin have the capacity to
mimic and bind to oestrogen receptors. 'Xenoestrogens' or oestrogen-like substances foreign to the
human body are endocrine disruptors. E levated levels of oestrogen can promote cell proliferation
which can lead to breast cancer and endometriosis. Women may be exposed to endocrine disruptors
through environmental contamination from industrial or agricultural processes; dietary exposures from
consuming contaminated fish or vegetables; in the workplace; traffic exhaust or drugs and
contraceptives containing synthetic oestrogens.
Female physiology poses increased risk
Women's physiology and role in society makes them bear the brunt of environmental toxins -- the so-
called ‘body burden’ or the amount of synthetic chemicals found in the human body. Physiological
differences between women and men, including differences in hormonal structure, mean that women
are susceptible to different health effects from exposure to toxins. Certain tissues in a woman's body
contain receptors that latch onto oestrogen molecules. When oestrogen molecules are bound to the
receptors, the cells of these ‘target tissues’ are stimulated to proliferate. The cells of the vagina, the
uterus and the breast all contain large numbers of oestrogen receptors, and grow in the presence of
oestrogen. Xenoestrogens bind to these receptors and disrupt the natural balance.
Because they derive from oil, x enoestrogens are fat-soluble and tend to accumulate in areas of the
body where fat content is high -- for example breasts, and may reside in the body for long periods of
time. Storage of toxins in fat is a problem of greater importance for women because of their higher
percentage of body fat and the hormonal changes that occur during menarche, menstruation,

pregnancy, lactation, and menopause. These can mobilise internal stores of pollutants many years
after the initial exposure. Bone loss is accelerated during menopause at which time bone mass may
decrease by 2-3% per year for several years. During this period, stored toxins may be released and
cause damage to the nervous system and other organs. This problem is worsened when a woman’s diet
is calcium-deficient because this deficiency accelerates mineral release from bone. Lead is the most
serious of several hazardous pollutants that affect bone, especially in countries like India that continue
to use leaded petrol.
In pregnant women, endocrine disruptors and harmful chemicals like lead and mercury can be passed
through the placenta, exposing the foetus, or through breast-feeding, exposing the infant to significant
levels of these chemicals. The tragic outcome of years of spraying endosulphan –an extremely
hazardous pesticide—on cashew plantations in Kerala is seen in the severely deformed babies. Besides
chemicals, radiation hazards have a deep impact on the health of women and their babies. Almost half
the women in villages around the Jadugoda uranium mine report disrupted menstruation, miscarriages
and babies with partially formed skulls, missing eyes or toes and fused fingers. Alarmingly high levels of
dioxin in breast milk portend an unhealthy future for infants of exposed mothers living near waste
dumps where dioxin levels are high.
Measuring Toxicity:
There is no legislative provision to link pesticide registration to setting MRLs. IA mandates
registration, but PFA mandates MRLs. Of the 180 pesticides currently registered, MRLs have
been set only for 71. In other words, more than 60 percent of pesticides currently registered
have no MRLs.
The new standards set were as follows:
• No pesticide residue in any individual unit of food/drink should exceed 0.0001 mg/litre
• Total pesticide residues cannot be more than 0.0005 mg/litre.
The value commonly used to measure acute toxicity is LD 50 (a lethal dose in the short term; the
subscript 50 indicates the dose is toxic enough to kill 50 per cent of lab animals exposed to the
chemical). LD 50 values are measured zero onwards; the lower the LD 50 the more acutely toxic the
pesticide. To illustrate, we compare DDT — most used in India up to the early 1990s — with
monocrotophos, currently most used. DDT’ S LD 50 is 113 mg/kg; monocrotophos, 14 mg/kg. But let us
never forget that lower LD 50 means higher acute toxicity.
Who invented the idea of an LD50?
In 1927, J.W. Trevan attempted to find a way to estimate the relative poisoning potency of drugs and
medicines used at that time. He developed the LD50 test because the use of death as a "target" allows
for comparisons between chemicals that poison the body in very different ways. Since Trevan's early
work, other scientists have developed different approaches for more direct, faster methods of
obtaining the LD50.
What are some other toxicity dose terms in common usage?
LD01 Lethal dose for 1% of the animal test population
LD100 Lethal dose for 100% of the animal test population
LDLO The lowest dose causing lethality

TDLO The lowest dose causing a toxic effect
LD50/LC50: A common measure of the acute toxicity is the lethal dose (LD50) or lethal concentration
(LC50) that causes death (resulting from a single or limited exposure) in 50% of the treated animals,
known as the population. LD50 is generally expressed as the dose, in milligrams (mg) of chemical per
kilogram (kg) of body weight. LC50 is often expressed as mg of chemical per volume (e.g., litre (L) of
medium (i.e., air or water) the organism is exposed to. Chemicals are considered highly toxic when the
LD50/LC50 is small and practically non-toxic when the figure is large, (some people have difficulty
getting their heads round this, as they think that if the number is large, then so is the toxicity, not
so...!). However, the LD50/LC50 does not reflect any effects from long term exposure (i.e., cancer,
birth defects or reproductive toxicity) that may occur at levels below those which cause death, these
are covered by things such as OEL (Occupational Exposure Limit) which we are not about here.
What does LD50 mean?
LD stands for "Lethal Dose". LD50 is the amount of a material, given all at once, which causes the death
of 50% (one half) of a group of test animals. The LD50 is one way to measure the short-term poisoning
potential (acute toxicity) of a material.
Toxicologists can use many kinds of animals but most often testing is done with rats and mice. It is
usually expressed as the amount of chemical administered (e.g., milligrams) per 100 grams (for smaller
animals) or per kilogram (for bigger test subjects) of the body weight of the test animal. The LD50 can
be found for any route of entry or administration but dermal (applied to the skin) and oral (given by
mouth) administration methods are the most common.
What does LC50 mean?
LC stands for "Lethal Concentration". LC values usually refer to the concentration of a chemical in air
but in environmental studies it can also mean the concentration of a chemical in water. For inhalation
experiments, the concentration of the chemical in air that kills 50% of the test animals in a given time
(usually four hours) is the LC50 value.
Why study LD50's?
Chemicals can have a wide range of effects on our health. Depending on how the chemical will be
used, many kinds of toxicity tests may be required.
Since different chemicals cause different toxic effects, comparing the toxicity of one with another is
hard. We could measure the amount of a chemical that causes kidney damage, for example, but not all
chemicals will damage the kidney. We could say that nerve damage is observed when 10 grams of
chemical A is administered, and kidney damage is observed when 10 grams of chemical B is
administered. However, this information does not tell us if A or B is more toxic because we do not
know which damage is more critical or harmful. Therefore, to compare the toxic potency or intensity
of different chemicals, researchers must measure the same effect. One way is to carry out lethality
testing (the LD50 tests) by measuring how much of a chemical is required to cause death. This type of
test is also referred to as a "quantal" test because it is measures an effect that "occurs" or "does not
occur".
Why are LD50 and LC50 values a measure of acute toxicity?
Acute toxicity is the ability of a chemical to cause ill effects relatively soon after one oral
administration or a 4-hour exposure to a chemical in air. "Relatively soon" is usually defined as a period
of minutes, hours (up to 24) or days (up to about 2 weeks) but rarely longer.

How are LD/LC50 tests done?
In nearly all cases, LD50 tests are performed using a pure form of the chemical. Mixtures are rarely
studied. The chemical may be given to the animals by mouth (oral); by applying on the skin (dermal);
by injection at sites such as the blood veins (i.v.- intravenous), muscles (i.m. - intramuscular) or into
the abdominal cavity (i.p. - intraperitoneal).
The LD50 value obtained at the end of the experiment is identified as the LD50 (oral), LD50 (skin), LD50
(i.v.), etc., as appropriate. Researchers can do the test with any animal species but they use rats or
mice most often. Other species include dogs, hamsters, cats, guinea-pigs, rabbits, and monkeys. In
each case, the LD50 value is expressed as the weight of chemical administered per kilogram body weight
of the animal and it states the test animal used and route of exposure or administration; e.g., LD50
(oral, rat) - 5 mg/kg, LD50 (skin, rabbit) - 5 g/kg. So, the example "LD50 (oral, rat) 5 mg/kg" means that
5 milligrams of that chemical for every 1 kilogram body weight of the rat, when administered in one
dose by mouth, causes the death of 50% of the test group.
If the lethal effects from breathing a compound are to be tested, the chemical (usually a gas or
vapour) is first mixed in a known concentration in a special air chamber where the test animals will be
placed. This concentration is usually quoted as parts per million (ppm) or milligrams per cubic metre
(mg/m3
). In these experiments, the concentration that kills 50% of the animals is called an LC50 (Lethal
Concentration 50) rather than an LD50. When an LC50 value is reported, it should also state the kind of
test animal studied and the duration of the exposure, e.g., LC50 (rat) - 1000 ppm/ 4 hr or LC50 (mouse) -
5mg/m3
/ 2hr.
Which LD50 information is the most important for occupational health and safety purposes?
Inhalation and skin absorption are the most common routes by which workplace chemicals enter the
body. Thus, the most relevant from the occupational exposure viewpoint are the inhalation and skin
application tests. Despite this fact, the most frequently performed lethality study is the oral LD50. This
difference occurs because giving chemicals to animals by mouth is much easier and less expensive than
other techniques. However, the results of oral studies are important for drugs, food poisonings, and
accidental domestic poisonings. Oral occupational poisonings might occur by contamination of food or
cigarettes from unwashed hands, and by accidental swallowing.
How do I compare one LD50 value to another and what does it mean to humans?
In general, the smaller the LD50 value, the more toxic the chemical is. The opposite is also true: the
larger the LD50 value, the lower the toxicity. The LD50 gives a measure of the immediate or acute
toxicity of a chemical in the strain, sex, and age group of a particular animal species being tested.
Changing any of these variables (e.g., type animal or age) could result in finding a different LD50 value.
The LD50 test was neither designed nor intended to give information on long-term exposure effects of a
chemical.
Once you have an LD50 value, it can be compared to other values by using a toxicity scale. Confusion
sometimes occurs because several different toxicity scales are in use. The two most common scales
used are the "Hodge and Sterner Scale" and the "Gosselin, Smith and Hodge Scale". These tables differ
in both the numerical rating given to each class and the terms used to describe each class. For
example, a chemical with an oral LD50 value of 2 mg/kg, would be rated as "1" and "highly toxic"
according to the Hodge and Sterner Scale but rated as "6" and "super toxic" according to the Gosselin,
Smith and Hodge Scale. It is important to reference the scale you used when classifying a compound.

It is also important to know that the actual LD50 value may be different for a given chemical depending
on the route of exposure (e.g., oral, dermal, inhalation). For example, some LD50s for dichlorvos, an
insecticide commonly used in household pesticide strips, are listed below:
• Oral LD50 (rat): 56 mg/kg
• Dermal LD50 (rat): 75 mg/kg
• Intraperitoneal LD50: (rat) 15 mg/kg
• Inhalation LC50 (rat): 1.7 ppm (15 mg/m3); 4-hour exposure
• Oral LD50 (rabbit) 10 mg/kg
• Oral LD50 (pigeon:): 23.7 mg/kg
• Oral LD50 (rat): 56 mg/kg
• Oral (mouse): 61 mg/kg
• Oral (dog): 100 mg/kg
• Oral (pig): 157 mg/kg
Differences in the LD50 toxicity ratings reflect the different routes of exposure. The toxicity rating can
be different for different animals. The data above show that dichlorvos is much less toxic by ingestion
in pigs or dogs than in rats. Using Table 1, dichlorvos is moderately toxic when swallowed (oral LD50)
and extremely toxic when breathed (inhalation LC50) in the rat. Using Table 2, dichlorvos is considered
very toxic when swallowed (oral LD50) by a rat.
Table 1: Toxicity Classes: Hodge and Sterner Scale
Routes of Administration
Oral LD50 Inhalation LC50 Dermal LD50
Toxicity
Rating
Commonly
Used Term
(single dose
to rats)
mg/kg
(exposure of rats
for 4 hours) ppm
(single application to
skin of rabbits) mg/kg
Probable Lethal
Dose for Man
1 Extremely
Toxic
1 or less 10 or less 5 or less 1 grain (a taste,
a drop)
2 Highly Toxic 1-50 10-100 5-43 4 ml (1 tsp)
3 Moderately
Toxic
50-500 100-1000 44-340 30 ml (1 fl. oz.)

4 Slightly Toxic 500-5000 1000-10,000 350-2810 600 ml (1 pint)
5 Practically
Non-toxic
5000-15,000 10,000-100,000 2820-22,590 1 litre (or 1
quart)
6 Relatively
Harmless
15,000 or
more
100,000 22,600 or more 1 litre (or 1
quart)
Table 2: Toxicity Classes: Gosselin, Smith and Hodge
Probable Oral Lethal Dose (Human)
Toxicity Rating or Class Dose For 70-kg Person (150 lbs)
6 Super Toxic Less than 5 mg/kg 1 grain (a taste - less than 7 drops)
5 Extremely Toxic 5-50 mg/kg 4 ml (between 7 drops and 1 tsp)
4 Very Toxic 50-500 mg/kg 30 ml (between 1 tsp and 1 fl ounce)
3 Moderately Toxic 0.5-5 g/kg 30-600 ml (between 1 fl oz and 1 pint)
2 Slightly Toxic 5-15 g/kg 600-1200 ml (between 1 pint to 1 quart)
1 Practically Non-Toxic Above 15 g/kg More than 1200 ml (more than 1 quart)
Can animal LD50 data be applied to man?
In general, if the immediate toxicity is similar in all of the different animals tested, the degree of
immediate toxicity will probably be similar for humans. When the LD50 values are different for various
animal species, one has to make approximations and assumptions when estimating the probable lethal
dose for man. Tables 1 and 2 have a column for estimated lethal doses in man. Special calculations are
used when translating animal LD50 values to possible lethal dose values for humans. Safety factors of
10,000 or 1000 are usually included in such calculations to allow for the variability between individuals
and how they react to a chemical, and for the uncertainties of experiment test results.
How should an LD50 value be used?

The LD50 can be used:
• As an aid in developing emergency procedures in case of a major spill or accident.
• To help develop guidelines for the use of appropriate safety clothing and equipment. For
example, if the dermal LD50 value for a chemical is rated as extremely toxic, it is important to
protect the skin with clothing, gloves (etc.) made of the right chemical-resistant material
before handling. Alternatively, if a chemical has an inhalation LC50 value which indicates that it
is relatively harmless, respiratory protective equipment may not be necessary (as long as the
oxygen concentration in the air is in the normal range - around 18%).
• For the development of transportation regulations.
• As an aid in establishing occupational exposure limits.
• As a part of the information in Material Safety Data Sheets. Remember, the LD50 is only a ball
park figure so that lethal toxicity can be compared. It says nothing about levels at which other
acute toxic, but non-lethal, effects might occur.
The LD50 is only one source of toxicity information. For a more thorough picture of the immediate or
acute toxicity of a chemical, additional information should be considered such as the lowest dose that
causes a toxic effect (TDLO), the rate of recovery from a toxic effect, and the possibility that exposure
to some mixtures may result in increasing the toxic effect of an individual chemical.
Analysis
The blood samples were analyzed with a widely and internationally used methodology for
Organochlorine pesticides with Electron Capture Detector and Organophosphorus pesticide with
Nitrogen Phosphorus detector using a capillary column.
A particular challenge in the detection and quantification of multiple pesticides in a single run derives
from the complex elution situation. Because many compounds coelute partially or completely, the SRM
transition speed must be fast enough to monitor many coeluting components while generating an
adequate number of data points for qualitative and quantitative analysis in addition to reliable
integration of overlapping chromatographic peaks. Analysis should include as many substances as
possible, requiring a method capable of acquiring several hundred SRM transitions in a single run. Given
that small changes in retention time may occur in cases of heavy matrix samples, the method of choice
should also require a minimal number of acquisition segments for multiple targets. In other words, the
method must be able to measure as many transitions as possible in one segment window without any
sensitivity loss.
To analyze hundreds of pesticides in one run, short dwell times and interscan times have to be used. As
a consequence, a memory effect of the collision cell, called "cross talk," can occur on some triple
quadrupole instruments. Multi-residue pesticide analysis requires a method with the inherent capability
of separating analytes from one another to facilitate individual identification and measurement. The
Codex Guidelines on Good Laboratory Practice in Pesticide Residue Analysis specify mass spectrometry
(MS) as the most appropriate technique for multi-residue pesticide analysis being capable of providing
both quantitative and qualitative data.9
In general, MS is coupled with a chromatographic separation
method to achieve simultaneous generation of retention time, ion mass/charge ratio and ion
abundance data.
Liquid chromatography-mass spectrometry (LC-MS) provides good supporting evidence, but offers
incomplete results since the generated spectra demonstrates little characteristic fragmentation. LC-MS
is also associated with matrix effects, requiring the use of standards to overcome them. High
performance liquid chromatography-mass spectrometry (HPLC-MS) is an improved liquid

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