We found 15 different pesticides -- a cocktail of 6-13 pesticides, all different -- in the 20 blood samples we tested from four villages in Punjab. What does this imply for public health? Can such plural contamination supress the immune system, in turn increasing cancer and other ailments?
To understand this, let us find out how science estimates how much of pesticide in blood is 'safe'. Does a safety threshold level exist? If yes, how do scientists -- and the industry -- compute it? As we delve into such questions, it becomes clear that science claims more, but understands much less. This, too, comes horrifically out in the open: humans are also victims of a criminal trespass by the pesticide industry.
Pesticides are toxins. But its makers say the exact dose differentiates between poison and remedy. So, regulators benchmark exposures into two types: short-term exposure which leads to acute-toxicity, and repeated or long-term exposure, which causes chronic toxicity; symptoms develop over time.
All pesticides are tested to establish toxicity -- a dose necessary to produce a measurable harmful effect -- usually established through tests on mice, rats, rabbits and dogs. Results are then extrapolated on humans, and safe exposure levels predicted.
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 establish chronic toxicity, animals receive a pesticide-laced diet from a very young age. This continues till they show chronic adverse affects whether carcinogenic in nature, or mutagenic or with definite impairment in the reproductive system. Such experiments have a purpose: determine a no-observable-effect-level (noael) of pesticide exposure -- a level in the total diet that causes no effect on test animals as compared to others maintained under unexposed conditions. Sometimes, it is not possible to deduce this number. Then, the safety mark is established at the point where the first, minutest, adverse effect appears. This is called loael, or "Lowest Observable Adverse Effect Level". noael / loael is expressed as pesticide exposure in milligramme per kilogramme of body weight per day (mg/kg bw/day).
ld50 and noael values are then extrapolated to determine safety values for humans, known as acute reference dose (aRfD) for acute toxicity and acceptable daily intake (adi) for chronic toxicity. aRfD and adi are arrived at by adjusting ld 50 and noael values downwards; usually, by a factor of 100 respectively: a division factor of 10 is used to allow for the possibility that humans are more sensitive than animals; another division factor of 10 is used to allow for differences amongst individual humans.
Toxicity apart, persistence is an important trait of a pesticide: this characteristic has compelled regulation. Older organochlorine pesticides, say ddt or bhc, were persistent: they are still found in water, soil and human blood even though their use was discontinued many years back.
To circumvent this problem, industry devised new pesticides: these degrade in the environment. For that reason, these have much less time to accomplish their job; so, they have to be far more toxic then their older, persistent, cousins. Contemporary pesticides kill pests with very small doses, and so are far more lethal.
Let's 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. In other words, the acute toxicity of monocrotophos is eight times higher than ddt . Moreover, monocrotophos has an adi of 0.00005 mg/kg: it is 10 times more chronically toxic than ddt (see table: Gen-next pesticides).
Similarly, chlorpyrifos -- also widely used in India -- is five times more chronically toxic than ddt.
It is understood that once ingested, pesticides accumulate in the body fat or pass through. Organochlorine pesticides, for instance, accumulate in body fat and blood lipids. These fat-soluble chemicals persist in the body for many years. Research traditionally concentrated on such pesticides. Then the pesticides that were persistent gave way to the more toxic ones. But even now, scientist are merely beginning to fathom what happens when these latter-day pesticides circulate and pass through humans.
The us- based Centre for Disease Control and Prevention (cdc) regularly conducts one of the most comprehensive biomonitoring programmes in the world -- the National Report on Human Exposure to Environmental Chemicals -- to aim to determine the chemical body burden of us residents and also investigate potential links to diseases. cdc's second report of January 2003 analyses blood and urine levels of 116 environmental chemicals. The sample population was studied from 1999 through 2000.
Five of the pesticides we tested for were those studied by the cdc. So, let's compare. To our horror we found the Punjab samples had far higher pesticide residues (S ee table: Horrific). For example, lindane residues in our samples were 600 times higher than the cdc study. Similarly, levels of dde and ddt in the Punjab samples were 35 times and 188 times higher than the us samples.
What does this mean? Are there any acceptable levels for these pesticides in blood? Says cdc's 2003 report: "The recommended limit value in blood for lindane has been established by various agencies and organisations. uk's benchmark guidance value is 35 nanomoles per liter (approximately 1,700 nanogramme/gramme of lipid)". The same lindane in Punjab villagers' blood samples was about three times this value.
These alarming results are only for 'persistent' organochlorines. Industry claims that the 'new' organophosphorous pesticides (ops) are low-dose, less persistent. It never mentions that low dose also means higher toxicity. Our tests also belie their claim that ops are less persistent. We found the supposedly low persistent op monocrotophos in 75 per cent of the blood samples. cse's pollution monitoring lab found another op, chlorpyrifos, in 85 per cent of samples, 70 per cent of which contained two more ops: phosphamidon and malathion. In fact, ops constituted more than 60 per cent of the total pesticide residues in the samples. Nothing unusual. After all, studies in the us and other parts of the world have found such pesticides in human blood. The point is: our study shows such contamination has reached alarming proportions.
ops have both high acute as well as chronic toxicity. The level of ops found in the Punjab blood samples we collected could be the case of both acute and chronic poisoning. For example, the average monocrotophos level found was 0.095 milligramme per litre (mg/l). Considering about 5 litres of blood circulate in an average human, every sample contained 0.475 mg of monocrotophos, on average, only in their blood. The aRfD (short term exposure limit for humans as per the World Health Organization/Food and Agriculture Organization, who/fao) of monocrotophos is 0.002 mg/kg bw/day. This means an average adult weighing 60 kg cannot exceed the acute exposure limit of 0.12 mg/day (0.002 mg/kg multiplied by 60 kg) for monocrotophos.
Shockingly, the blood samples alone contained 4 times more monocrotophos than the aRfD. This is significant if we consider the "known" properties of monocrotophos, not supposed to persist in the body and so, ideally, excreted soon. For monocrotophos to be present in the high amounts found in the blood samples, the regular exposure must have been high enough, perhaps far higher than the aRfD. Our findings clearly point out to such exposure among the people studied. And this was not just for monocrotophos. The level of chlorpyrifos found in the blood samples alone was more than 3 times the short-term exposure usepa limit. Clearly, this kind of exposure is unacceptable.
Pesticides are commonly used in Punjab. Thus, we cannot rule out chronic poisoning by ops as well. It is relatively clear chronic exposures to ops occur as a 'circulating dose'. People so exposed may excrete these chemicals quite quickly. But since op s are used widely, people get re-exposed; they carry them as part of their pesticide body burden. If this is the case, the people we took samples from could have been exposed to similar levels of pesticides year around -- disastrous!
Why? Because the chronic acceptable daily exposure limit for monocrotophos is just 0.00005 mg/kg bw/day. This means an adult of 60 kg can be exposed to no more than 0.003 mg/day of this pesticide. But we found average levels of 0.095 mg/l of monocrotophos in collected blood samples alone, 158 times more than the daily long-term safe exposure limit. And we are talking of residues only in blood.
Very little is known about the link between pesticide body burden and health impacts. Biomonitoring studies -- measuring chemicals in blood, urine, breast milk, fat, hair or other tissues -- do reveal that large amounts of synthetic chemical residues have infiltrated our bodies. Yet, industry argues there is no evidence these chemicals cause harm. Having chemicals in our bodies is unavoidable in modern times, they contend. They take refuge behind what they call a lack of 'authentic' epidemiological studies correlating disease to the invasion by a pesticide. Industry also finds it useful that there are many pesticides and chemicals involved in the assault. It makes it difficult to pinpoint blame. The conspiracy of denial continues.
But toxicological impacts of individual pesticides is stark. There is also no evidence that proves the safety of carrying a chemical body burden; in fact there is growing evidence to incriminate such burden. Biomonitoring research suggests that the chemical cocktail in our bodies could be linked to a host of afflictions: developmental disorders, fertility problems, neurological disorders and cancer, with exact effects varying person to person. In addition, virtually nothing is known about cumulative health impacts of dozens of chemicals present in the body at the same time.
So it is that, now, it is widely recognised that finding the exact effects of the chemical body burden is not the issue at all: identifying the cocktail of chemicals in human bodies and setting up regulatory systems to reduce the chemical body burden is more significant. The general premise is that, irrespective of their impacts, synthetic chemicals should not be allowed to trespass human bodies.
As biomonitoring results confirm the presence of pesticides in even occupationally unexposed population, the industry is at pains to defend its standard argument: "safe use" of pesticides poses no risk. But increasing evidence proves that they are horribly wrong. Many researchers, scientists and ngos now believe there should be a paradigm shift in the way pesticides are regulated. It's no more about monitoring pesticides in food commodities only. It's about checking the body burden and then regulating these toxins.
Body burden studies hold the key to a fool-proof system to regulate the use of pesticides and other chemicals. This view is also gaining ground among policymakers in the West -- albeit slowly. For example, in 2003 the uk Royal Commission on Environmental Pollution stated, "where chemicals are found in elevated concentrations in biological fluids such as breast milk, they should be removed from the market immediately". In fact, policymakers in New Zealand and the state of Tasmania in Australia are now debating Chemical Trespass Bills which will render illegal the ingress of agricultural chemicals into the human body and also facilitate the recovery of damages.
Similar concerns are also driving action elsewhere. On April 27, 2003 the us Supreme Court affirmed the rights of consumers, workers and farmers to sue pesticide manufacturers when their product causes harm. The ruling strikes down the pesticide industry's persistent claims that registration of a pesticide under the us federal pesticide law automatically shields manufacturers from damage claims. The judgement also overrules the pesticide industry's claims that the Federal Fungicide Insecticide and Rodenticide Act, 1948 (thereafter amended many times) pre-empts local and state liability statutes
Assigning primary responsibility to pesticide manufacturers is an efficient way to address the problem of chemical trespass. So far, little penal action has been possible against these manufacturers, even when a clear link has been established between their product and its adverse health implications. To be effective, the modern regulatory system has to consider the chemical body burden and hold manufacturers of these toxins accountable.
Biomonitoring has not yet been institutionalised in India; the government has no specific programme for it. However, a few public as well as private institutions have conducted tests to find pesticide residues in human blood, fat and milk. In the past, Indian researchers have found ddt and bhc levels in the blood of Indians to be among the highest in the world. For example, a 1992 study published in the journal, Science of Total Environment found ddt levels to be as high as 7.17 parts per million in blood samples. However, most Indian studies on pesticide residues in humans are restricted to older organochlorine pesticides such as ddt and bhc. We have not come across any research on the presence of ops in the blood of Indians.
Clearly the new burden that modern India is carrying -- as Punjab clearly exemplifies, in our study that could be called the proverbial tip of the iceberg -- needs to be examined by its scientists. Doing anything less would be negligent.
-- Kushal Pal Singh Yadav