HEALTH IMPACTS OF PESTICIDES
- A cocktail of three to six pesticides found in all samples
- Lindane — a confirmed carcinogen — was found at an average concentration of 5.5 ppb, which is 54 times higher than the BIS standard (finalised but not notified) for individual pesticides in soft drinks (0.1 ppb)
- In one sample of Coca-Cola bought in Kolkata, lindane was as high as 14 ppb, which is 140 times higher than the BIS standard
- Chlorpyrifos, a known neurotoxin also known to breach the placenta, was found in all samples at an average concentration of 4.8 ppb, which is 47 times higher
- A Coca-Cola sample bought in Mumbai, manufactured in Thane, contained 20.4 ppb of chlorpyrifos: this is 200 times higher than the BIS standard for an individual pesticide. Heptachlor, banned in India, was found in 71 per cent of the samples, at levels which are four times the BIS standards
- The average amount of pesticide residues found in all samples was 11.85 ppb, which is 23 times higher than the BIS standards for total pesticides in soft drinks (0.5 ppb)
- Pepsi Cola, the flagship brand of PepsiCo India, on an average contained 15.2 ppb pesticide residues; this is 30 times the BIS standards. Coca-Cola, the flagship brand of Coca-Cola India, on an average contained 13.4 ppb pesticide residues; this is 27 times the BIS standards
- The average pesticide residues in all brands of PepsiCo was 12.7 ppb. This is 25 times the BIS standards
- The average pesticide residues in all brands of Coca-Cola India was 11.05 ppb. This is 22 times the BIS
standards
LINDANE
Lindane is absorbed through respiratory, digestive or cutaneous routes and accumulates in fat tissues. It damages human liver, kidney, neural and immune systems and induces birth defects cancer and death. Chronic administration results in endocrine disruption in birds as well as in mammals.
Treatment with 1-40 mg of lindane/kg of body weight disrupts testicular morphology,decreases spermatogenesis,inhibits testicular steroidogenesis, reduces plasma androgen concentrations and may adversely affect reproductive performance in males.In females lindane disrupts the estrous cycle, reduces serum estrogen and progesterone levels decreases sexual receptivity.
There has been a link of Lindane to immune system.Lindane is a potent carcinogen. Rats exposed to gamma HCH showed evidence of liver cancer.(Agency for Toxic Substances and Disease Registry (ATSDR)(1989) Public Health Statement for
Hexachlorocyclohexane.Atlanta,GA:US Department of Health and Human Services.).
Chronic exposure to Lindane has been liked to increase in the risk of cancer of the aerodigestive tract and strong genotoxic effects on human tonsillar epithelium.(Source:J.Soc Biol,2002 196(4):339-48)
Lindane was found to be estrogenic to female rats and mice,and also caused the testes of male rats to become atrophied.Seminiferous tubules and Leydig cells (important for production of sperms) were completely degenerated at dozes of 8 mg/Kg/day over a 10-day period (Gallo M A and Lawryk NJ (1991)Organophosphorus Pesticides.In Handbook of Pesticide Toxicology.Hayes,W. J.,Jr.and Laws,E.R.,Jr.,Eds.Academic Press,New York,NY pp 3-5).
The absorption of high doses of gamma -HCH is particularly toxic for the central nervous system and for the female and male reproduction apparatus in mammals where lindane is considered as an endocrine disruptor. Lindane is highly lipophilic and incorporates into biological membranes according to the following sequence:mitochondria,sarcoplasmic,reticulum,myelin,brain microsomes,erythrocytes.
Lindane exerts a stimulating action on synaptic transmission and inhibits the
chloride current activated by gamma-amino butyric acid (GABA)of many muscular
and nervous preparations by interacting with the receptors GABA -chloride channel
complex. It seems to affect calcium homeostasis of many tissues.
Lindane affects the excitable membranes and the cardio circulatory system.These alterations (may) represent a potential risk for human health .(Sauviat MP,Pages N (2002) Cardiotoxicity of lindane,a gamma isomer of hexachlorocyclohexane.J Soc Biol 2002 196 (4):339-48).
DDT
DDT (dichlorodiphenyltrichloroethane) and its metabolites have been linked
to altered sexual development in various species, to a decrease semen quality
and to increased risk of breast cancer in women. (Sharpe
RM,et al 1993;Carlsen E et al ,1992; Stone R et al ,1994).
DDT and its metabolites have also been shown to mimic estrogen ,binding
to and activating the estrogen receptors (ER's) thereby often producing estrogen
like effects (Jaga
K, (2000). What are the Implications of the interaction between DDT and Estrogen
Receptors in the body. Med Hypothesis 54: 18-25). They may alter a number
of harmful estrogen-regulated health effects in humans such as breast cancer
(Coceo
Petal (2002) Cancer mortality and environmental exposure to DDE in United States.
Environ Health Perspect ive 108: 1-4), spontaneous abortion
(Korrick
SA, etal (2001) Association of DDT with Spontaneous Abortion : a Case Control
Study Avn Epidemiol 11 : 491-496), reduced bone mineral density (Beard J
et al ,2000). DDT and its metabolites because of their lipophilicity
and long half lives accumulate in the food chain. Their weak oestrogenic
effects may result from altered metabolism and competition for binding to cytosolic
and nuclear receptors of steroid hormones.(Levine
R. Recognized and possible effects of pesticides in humans. In: Hayes WJ Jr,
Laws ER Jr, eds. Handbook of pesticide toxicology. Vol 1. General principles
. San Diego: Academic Press, 1991:275-360 ).
- DDT reportedly induces cancer in animals,mimics estrogen activity,induces
antiandrogen effects, and impairs Natural Killer (NK)cells and T lymphocyte
responses.
- Occupational exposure to insecticides resulted in frequent infections and
immunological abnormalities DDT,dichlorodiphenyldichloroethylene
(DDE),and dichlorodiphenyldichloroethane (DDD)in blood levels have been associated
with several immune parameters in patients occupationally exposed to insecticides.
- The majority of 49 patients who worked as farmers or farmhands in the former
German Democratic Republic,were contaminated with more than 1 chemical--most
commonly DDE,PCBs,and HCB and 80%of them had been exposed for more than 20 years.
(Daniel
V, et al (2002) Associations of dichlorodiphenyltrichloroethane (DDT) 4.4 and
dischlorodiphenyldichloroethylene (DDE) 4.4 blood levels with plasma IL-4. Arch
Environ Health Nov-Dec; 57(6):541-7).
- Comparison of blood levels of HCB and total DDT in 159 women with breast cancer
and 250 presumably healthy controls showed that mean levels of total DDT and
HCB were significantly higher for breast cancer patients than for controls.
No differences in serum levels of total DDT or HCB were found between estrogen
receptor positive and estrogen receptor negative patients with breast
cancer which implies that persistent pollutants may occur in higher
concentrations in blood samples from breast cancer patients from controls.(Charlier
C, et al (2003) Breast cancer and serum organochlorines residues Occup Environ
Med, May; 60 (5):348-51 )
- There are mixture effects even when each mixture component is present at concentrations
that individually produces insignificant effects. Lifetime treatment of mice
with DDT induced liver tumours in a doze related manner and the tumors included
overtly metastasizing hepatoblastomas (Hoyer
AP et al (1998) Organochlorine exposure and risk of breast cancer Lancet, 352:1816-1820.). Main metabolites of DDT (pp ’DDE and pp ’DDD)are both carcinogenic
.Exposure to DDE resulted in high incidence of liver tumors in
both male and female mice. The combined exposure to DDE and DDD resulted in
a marked increase and early appearance of liver tumors in both sexes (Turosov
VS, Day NE, Tomatis L, Gati E, Charles RT (1973) Tumors in CFI mice exposed
for six consecutive generations to DDT. J. Natl. Cancer Inst 51: 983-997
).
- Mixture of 4 organochlorines (op'DDT,pp'DDE, -BHC and pp'DDT) acted
together to produce proliferative effects in MCF-7 human breast cancer cells
and the combined effect was additive (Gertrudis C et al 2001).A study
suggests that exposure to a mixture of DDT,HCH and endosulfan and decreased
fertility in
males,an increase in birth defects and in neonatal deaths (Rupa DS,1991). Detoxification
processes both in humans and animals involve conversion of DDT to less toxic
acetate;little is known about variations from person to person in these detoxification
mechanisms,and even less about intermediate metabolism concerned. Regardless
of detoxification mechanisms,DDT is stored cumulatively in body fat and excretion
is extremely slow even after intake ceases. (Smith
MI (1946) Accidental Ingestion of DDT , with a note on its metabolism in Man.
J.AM.A, 131:519-520 Stone R. (1994) Environmental estrogens stir debate. Science
265 :308-10.)
CHLORPYRIFOS
Chlorpyrifos,one of the most widely used organophosphorus pesticide has been
reported to be a developmental neyurotoxicant specifically targeting the immature
brain.(Barone
S, Das KP, Lassiter TL, White LD (2000) Vulnerable process of nervous system
development. A review of markers and methods. Neurotoxicology 21: 15-36).
Fetal and childhood exposure to chlorpyrifos has raised concerns about developmental
neurotoxicity. Exposure to chlorpyrifos resulted in adverse effects on brain
cell development and cholinergic biomarkers
Neonatal rats were found to be more sensitive to chlorpyrifos than the fetal
rats and animals exposed prenatally developed behavioral deficits in adolescence
and adulthood. (Qio
D, Seidler FJ, Tate CA, Cousins MM, Slotkin TA(2003) Fetal chlorpyrifos exposure:
adverse effects on brain cell development and cholinergic biomarkers emerge
postnatally and continue into adolescence and adulthood, April 111(4):536-44).
Developmental neurotoxicity of chlorpyrifos is thought to involve both neurons
and glia,increasing the vulnerability of the developing brain.The vulnerability
increases from the gestational exposure through later periods of development
which glial neuronal interactions influence brain architectural,circuitary and
function.Exposures occurring during childhood are as important as those occurring
prenatally.
Chlorpyrifos is a suspected neuroterratogen .
Recent findings suggest that chlorpyrifos has a shifting cellular target,initially
impairing the development of neurons and subsequently affecting the glia, which
develop much later.(Garcia et al 2001,2002).It was evaluated for potential
developmental toxicity in rats and was found to show fetotoxic and
terratogenic effects at maternal doze of 25 mg/kg per day,a doze
that also produced maternal toxicity.Fetal weight and viability were decreased
and fetal death and early resorption increased at this doze.(Farag
AT, El Okazy AM, El Aswed AF(2003) Developmental toxicity study of chlorpyrifos
in rats. Reprod Toxicol March-April;17(2):203-8).Studies carried out to
evaluate potentiel toxicological effects of chlorpyrifos in rats showed that
repeated exposure to subthreshold dozes of chlorpyrifos may lead to growth retardation,behavioural
abnormalities and muscle weakness.(Terry AV Jr,Stone JD et al (2003)Repeated
exposures to subthreshold dozes of chlorpyrifos in rats:hippocampal damage,impaired
axonal transport,and deficits in spatial learning.J.Pharmacol Exp Ther ,,Apr;305
(1):375-84.)
Chronic exposure to chlorpyrifos has been shown to cause immunological
change .
Comparison of chronic health complaints of twenty-nine individuals exposed to
chlorpyrifos with respect to peripheral lymphocyte phenotypes;autoantibodies
(nucleic acids and nucleoproteins,parietal cell,brush border, mitochondria,smooth
muscle,thyroid gland,and central nervous system/peripheral nervous system myelin);
mitogenesis to phytohemagglutinin and concanavillin and compared with 3 control
groups (i.e.,1 positive 2 negative)showed an increase in CD 26 expression,a
decrease in percentage of CD5 phenotype,decreased mitogenesis in response to
phytohemagglutinin and concanavillin,and an increased frequency of autoantibodies.The
alterations in these peripheral blood markers were unaffected by medication,
age, sex, or season. (Thrasher
JD, Heuser G, Broughton A (2002) Immunological abnormalities in humans chronically
exposed to chlorpoyrifos. Arch Environ Health, May-Jun, 57(3):181-7)
Chlorpyrifos toxicity becomes acute if transformed to chlorpyrifos
oxon ,which is a potent anticholine esterase,1000 times more toxic
than chlorpyrifos.Active chlorine dispersed in water causes rapid abiotic transformation
of chlorpyrifos to chlorpyrifos oxon.Chlorination is commonly used for treatment
of domestic water supplies which is a new concern about the safety of domestic
use of chlorpyrifos products. (Wu
J et al ,2003).The effects of chlorpyrifos and its major metabolite
chlorpyrifos oxon have been studied in two in vitro models,neuronotypic and
gliotypic C6 cells.Chlorpyrifos inhibited DNA synthesis in both cell lines,but
had greater effect on gliotypic cells.Chlopyrifos oxon,the active metabolite
that inhibits cholinesterase ,also decreased DNA synthesis
in PC-12 and C-6 cells with a preferential effect on the latter. Diazinon also
inhibits DNA synthesis with preference towards C-6 cells but is less effective
than chlorpyrifos (Qiao
D et al ,2001).
MALATHION
Malathion,a known cholinesterase inhibitor, responsible
for the hydrolysis of body choline esters,including acetylcholine at cholinergic
receptors.Primary site of action in insects is nervous system.It was found to
induce progression of malignant transformation in
epithelial cells in the rat mammary glands.It has been shown to induce changes
in the epithelium of rat mammary glands,influencing the process of carcinogenesis;
such alterations occur at the level of nervous system by increasing the cholinergic
stimulation (Vladimir
T et al ,2002). Malathion induces alterations in actin cytoskeleton
and in cell adhesion of cultured breast carcinoma cells.(Cabello
G et al 2003). It has been reported to induce a slight increse in
the incidence of chromosomal aberrations in bone marrow cells of
rats exposed in vivo. (Kawachi T et al ,1980).Malathion caused a significant
increase in sister chromatid exchange in human foetal lung fibroplasts after
a single doze of 40 ｵg/l or a double doze of 20 g/l.
(Nicholas
AH et al ,1979). (Cabello G,2003).
In contrast to potent carcinogens,which induce mammary carcinomas in 100 per
cent of intact females,parathion and malathion induced 14.3 and 24.3 per cent
of mammary carcinomas.Type of tumors induced had papillary adenmatous patterns
and ductal carcinomas with cribiform pattern (Willings
SR et al , 1975). Malathion incorporated through epithelium of skin,mouth
and respiratory tract,are activated in the liver by enzymatic processes producing
malaoxon.(Silman I,and Futerman A.,1987).It also has been shown to cause birth
defects in a variety of wildlife and at levels lower than other
pesticides.When administered to adult animals,malathion and related thiophosphonates
stimulate,and subsequently inhibit the nicotinic sites in skeletal muscle,resulting
in muscle weakness and paralysis. Neonates (newborn babies)are far more sensitive
to these agents than adults,mainly because of a slower rate of detoxification
of the metabolite (the metabolite in this case would be the liver breakdown
product of malathion –malaoxon which has been shown to be far more toxic
than malathion itself .(Source:Teratology,36:7-9,1987)
It was found to cause DNA abnormalities at all doses (0.02,0.2,2 and 20 ug/ml when added to human blood cells drawn from three healthy non-smoking men,aged 23,24 and 25.It causes a dose-dependent increase in chromosomal aberrations as well as sister chromatid exchanges in human leukocyte cultures.A dose dependent decrease in mitotic index was also observed which suggests that malathion is a mild mutagen and at higher concentrations it might cause genotoxicity in humans.(Source :Mutation Research,301:13-17,1993).
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