Contact for more information
Herbicides/Toxics - Updates to March 2005Aug 06: Hancock pollutes Geelong Drinking Water with Hexazinone for 18 months (and counting) Environmental groups call for bans on aerial spraying of pesticides Modes of Actions of herbicidesNightmare Unfolding in TasmaniaBluegum plantation insecticidesAtrazine and Hexazinone incident that killed 100 old growth redgum trees at Rosedale between 2000 and 2002.FSC Board Committee Decision Regarding Simazine Use in Victorian Plantations 3/11/03Chemical Policy of the Forest Stewardship CouncilHistorical data on 2,4,5-T use in Victorian PlantationsThe Continuing Health Problems Associated with 2,4,5-TChlorinated PesticidesTip of the iceberg (March 03)Water supplies and towns downstream of Hancock plantations (update)Plantations, Gold Mining and Mercury pollution
See Previous Herbicides Updates Atrazine and Hexazinone (Forest Mix WDH*) incident that killed 100 old growth redgum trees at Rosedale between 2000 and 2002. Friends Block Background 1 The site Friends Block (now owned by Grand Ridge Plantations (GRP) is located approximately 6km south of Rosedale. The district has a long grazing history. The site receives roughly 700mm of rain per year and is about 50m ASL. The landform is gently undulating to flat, with locally dissected drainage ways, or on flatter parts, shallow irregularly scattered depressions. The parent material is unconsolidated alluvial deposits of the late Pliocene age. The soils are a yellow duplex textured soil, with a loamy sand surface horizon over a yellow-brown mottled and generally dense clay. The block is about 450ha in size. 2 Past activities In 2000, the Friends Block was site prepared and planted in Pinus radiata by Australian Paper Plantations. The site had in excess of 100 old Red Gum trees on site, which were deliberately protected and left intact at time of site preparation and planting. A different herbicide was used to that used normally, which was believed to have a lesser effect on native trees. No herbicide was sprayed around the native trees but this appears to have been inadequate protection. On this block we applied "Forest Mix WDH*" @ 7.2Kg/Ha. Apparently, following herbicide application a strong rain event occurred, resulting in water from the general establishment area pooling around the base of the native trees. The water was slow to get away due to the duplex nature of the soil.
March 2003: Poisoned redgums - Friends Block 3. Unacceptable outcome Unfortunately, many of the Red Gums on the Friends Block have died since the site was established. This was brought to the attention of GRP in late 2002. The patterns of tree death have been investigated, and there are some parts of the block that have had very few deaths, whereas other parts have been heavily affected. There doesn't appear to be any patterns of death that can be related to topography or location within the block. It would appear that the combined effect of herbicide, cultivation and fertilisation has caused the rapid death of most of these trees. It is likely that the herbicide was the main factor. GRP has undertaken additional investigations including, analysis of the leaves of alive trees in the block for chloride, an analysis of the dam water for chloride and herbicide and an analysis of the soil for residual herbicide levels. These investigations have failed to turn up any additional information and there was no residual herbicide found in soil or water. 4. GRP response After the purchase of the Australian Paper business, GRP worked with the Regulatory Authority, Wellington Shire, in an attempt to mitigate the impact of the loss. Approximately 10,000 trees (local redgum and lightwood) have been planted in a biolink that stretches for 3 km along the main drainage line in the block. The biolink adjoins native vegetation at each end. This involved the removal of recently planted pine, fencing of the area, planting and tree guarding. The trees are currently about 50cm tall and growing well. The block is fenced and gated and signs have been erected to discourage any firewood getters. The redgums which have died, have hollows and must be retained for hollow nesting fauna. The Rosedale Historical Society, who have taken an interest in this issue have been kept informed of developments. *Forest Mix WDH is made by Macspred Pty Ltd (Ballarat). Active Contituents: 210 g/kg Hexazinone and 620 g/kg Atrazine used at a rate of 7.2 kg/ha. FSC Board Committee Decision Regarding Simazine Use in Victorian Plantations 3/11/03 (Background in April 2003, Hancock Victorian Plantations approached the FSC in terms of gaining a derogation for the continued use of the herbicide Simazine in its hardwood 'plantations' in Gippsland - what follows is the FSC judgement in terms of this derogation) FSC Board Committee Decision: Simazine may be used in Victoria, Australia, for the residual pre-emergent control of grass and broadleaved weeds in Eucalypt plantation establishment, until September 2006, and subject to the following conditions: 1. A 'Pesticides Advisory Group' which consists of technical advisers and which has the support of key FSC stakeholders in Victoria and environmental, social and economic members of the interim Australian NI shall be established by the FSC Australia Contact Person prior to any application of simazine by FSC certificate holders. 2. The role of the Pesticides Advisory Group shall be to provide guidance on the conditions attached to this derogation, and to review the results of monitoring carried out by certification bodies of certificates applying the derogation. Certificate holders shall make all necessary information available to members of the Advisory Group to allow them to meet these objectives. 3. Until the Pesticides Advisory Group gives clarifying guidance, there shall be no application of simazine in domestic supply water catchments. 4. Simazine shall not be applied on sites with conditions in which simazine can move off-site or accumulate in water courses. Until the Pesticides Advisory Group gives clarifying guidance, there shall be no aerial application of simazine in certified operations. 5. Where simazine is used there shall be buffers around the edges of sites and along drainage lines to ensure there is no spray drift, contamination of waterways, or off-site impact on native vegetation. 6. The Pesticides Advisory Group shall provide specific guidance to be followed with respect to: 6a. pre- and post- application monitoring of water courses, buffers, native vegetation and soils in catchments where simazine is applied; 6b. determination of sites, soils and catchments where it is not appropriate to apply simazine; 6c. the use of alternative chemicals that are not on the FSC prohibited list and have a lower risk of negative on- and/or off- site environmental impacts; 6d. determining the "trigger value" for simazine and procedures to be followed when monitoring shows the trigger value has been exceeded or when simazine is detected in waterways; 6e. appropriate application methods, in particular under what, if any, circumstances aerial application is acceptable. 6f. appropriate controls under which simazine may, if at all, be applied in domestic water supply catchments. 7. The policies and procedures of certifications applicants shall be evaluated and confirmed by the certification body prior to the issue of a certificate. Re: Simazine derogation (FSC-GUI-30-603) On 3rd November 2003 the FSC Board Committee on Chemical Pesticides agreed to permit a derogation for the use of simazine in Victoria, subject to a number of conditions. The decision and the associated conditions are described in the FSC document FSC-GUI-30-603. One of the conditions requires that a 'Pesticides Advisory Group' should be set up by the FSC Australia Contact Person to provide advice, prior to the application of simazine by any FSC certificate holder. The role of the Pesticides Advisory Group will be to provide advice on the application of the derogation, and to review the results of monitoring when simazine is used under its conditions. For this purpose the Pesticides Advisory Group is designed to consist of technical advisors and to have the support of stakeholders and FSC members in Victoria. During the review of the simazine derogation request it was clear that it would be highly useful if a Pesticides Advisory Group could be established to provide advice on any further derogation requests in Australia. This would ensure that derogation requests could be scrutinised by experts in Australia, prior to submission to FSC, and improve the quality and timeliness of the evaluation. There would be obvious advantages if the Pesticides Advisory Group set up to provide advice on simazine use in Victoria could go on to provide further advice on subsequent chemicals issues in the context of FSC certification in Australia as a whole. For further information, please contact Mr Tim Cadman, FSC Contact Person in Australia (tcadman@certifiedforests.org.au). Matthew Wenban-Smith (Head of Policy and Standards Unit - Forest Stewardship Council, Bonn Germany). Herbicide Regimes - March 2003: Hancock Watch has recently been given information pertaining to the quantity of herbicides sprayed in certain Hancock plantations in the Gippsland Region. This data was provided by Gippsland Water. Information is incomplete and doesn't give an indication of the full story associated with herbicide use by the company. Nevertheless it does shed some light on this important issue. Hancock are currently attempting to get their Victorian operations certified by the Forest Stewardship Council. FSC requires that companies reduce their herbicide regimes and ban the use of certain chemicals. We call on Hancock to publicly release all details of herbicide applications over their entire asset base. If we are not privy to this information then that is an unacceptable outcome - especially if herbicides are aerially dropped into peoples drinking water. The following links will provide information relating to plantations and their herbicide regimes over the past few years. Also see March 03 updates with information pertaining to a herbicide pollution incident which has killed old growth redgums in Central Gippsland. Incomplete Spray Regimes can be found at (plantations inside domestic water catchments highlighted in blue); 93-72, 93-73, 93-82, 93-89-1, 93-90-1, 93-97, 93-106, 93-108, LEGL93-118, 93-119, LEGL 93-120
Water Supplies Update November 2006:
Water supplies most likely to be impacted by Hancock activities (in red): For more detailed information on these potentially impacted water supplies, please go to connecting links: http://www.hancock.forests.org.au/directory/regional.html
|
| Variable Buffer width Buffer quality Stream length Plantation area Catchment area Catchment area ratio Application rate | All Sites (n=26) -0.547** -0.390* -0.493* -0.582** -0.640*** 0.707*** -0.132 | Plantation streams (n=11) -0.791** -0.529 -0.478 -0.515 -0.724* 0.693* 0.147 |
Receiving/Bordering streams (n=15) -0.505 0.158 -0.710** -0.679* -0.675* 0.142 -0.208 |
When data for streams which bordered plantations and/or received drainage from plantation streams (receiving streams, n=15) were analysed, there were significant negative correlations with stream length, plantation area and catchment area but not with buffer strip width (Table 1). Atrazine concentrations in receiving streams on the day of spray were not significantly correlated with those found in plantation streams which drained into them (r=0.561. p=0.14. n=8).
First rain and one month after spraying
Significant correlations were found between atrazine concentrations following the first rain event and buffer strip width, stream management area and catchment area ratio (Table 3). Marginal correlations were found with plantation catchment area and soil erosion class. Significant correlations were found between atrazine concentrations one month after spraying and all variables except soil erosion class and plantation slope (Table 3). A marginal correlation was found with soil erosion class.
Median concentrations at the first rain event after spraying for streams with -<10, 20 and 30 m buffers were 48.0, 36.4 and 3.6 ug/L (n=5, 7, 8) respectively. One month after spraying, the median concentrations were 25.0, 5.6 and 1.5 ug/L (n=5, 7, 9), at these buffer widths, respectively. Thus, only 30m buffer strip widths were associated with median atrazine concentrations between 20 ug/L at all times following spraying.
Highly significant positive correlations were also found between concentrations on the day of spray and concentrations at the same sites after the first rain event and the first month after spraying. Concentrations on the day of spray predicted 63.4 and 63.0% of the variance on the concentrations after the first rain event and the first month, respectively. Multiple linear regression against all independent variables showed that no other site variable improved this relationship (Table 2). Site variables alone were only able to predict 31.2 and 41.2% (stream catchment area) of the variance in atrazine concentration data on these two occasions, respectively. Thus, atrazine concentrations for up to one month after the day of spray were principally dictated by the extent of contamination on the day of spray itself and were only marginally affected by site characteristics.
Table 2. Regression equations describing atrazine concentrations
on the day of spray, 1st rain event after spraying and one month after
spraying (y in ug/L, all In(x+1) transformed) against site variables,
derived by multiple linear regression. CAR = catchment area ratio, PCA
= plantation catchment area.
| Date Day of Spray All sites Plantation streams Receiving/ bordering streams |
Equation y=2.977 + 3.047*(areasin CAR) - 3.611*In(PCA+1) y=7.670 - 1.544* (In[buffer width+1]) y=15.592 - 3.429*In([buffer width+1]) - 3.780*In(PCA+1) |
n 26 11 15 |
r (adj.) 0.56 0.58 0.52 |
ANOVA P <0.0001 0.004 0.013 |
| 1st Rain after spraying All sites |
y=1.184+0.451*(In[day of spray concentration+1]) |
21 |
0.63 |
<0.0001 |
| 1st month after spraying All sites All sites |
y=0.303+0.422*(In[day of spray concentration+1]) y=2.922-0.747 (In[catchment area+1]) |
21 24 |
0.63 0.41 |
<0.0001 0.0004 |
Peak (day of spray) pyrethroid concentrations were obtained on six
occasions, ranging from <0.01 to 0.50 ug/L. These concentrations were
significantly negatively correlated with buffer strip width (Table 4),
but not with any other site variable. A multiple linear regression model
of peak pyrethoid concentrations contained only buffer strip width as
a variable, explaining 71.6% of the variance in the data...
Discussion
Buffer strips are used along streams for a variety of reasons, particularly for the protection of water quality against the adverse effects of soil movement. The use, inadvertent or intentional, of buffer strips to protect stream water from contamination by pesticides on the day of spray is a direct result of the practical inability of both ground-based and aerial spraying operations to contain the drift of spray droplets after release. The lateral spread of a spray cloud in open terrain is determined by three principle factors: wind strength, droplet size and height of release (NSW 1986, McNeil, Forestry Commission Tasmania, pers. comm.). Spraying in the present study was principally by helicopter under relatively uniform conditions with low windspeeds and good operational control (see Forestry Commission 1988). Only one of the plantations studied was sprayed from a light plane and this, combined with a complete lack of buffer strips and a high application rate (10kg/ha), resulted in the highest day of spray concentration of atrazine found in the study (58 mg/L). Overall, therefore, the principal variables which could significantly influence the extent of contamination of plantation stream water on the day of spray in this study were the width and quality (density) of buffer strip vegetation between the primary spray cloud and the stream bank.
Significant negative correlations between buffer strip width and atrazine concentrations on the day of spray were found for all streams, and particularly for those streams directly draining the plantations. No relationship was found with buffer strip quality, suggesting that width rather than vegetation density was the dominant factor. Some contamination was found at all buffer strip widths on the day of spray, and the concentrations were highly variable. This variability is likely to be dictated by the unpredictability of aerial drift contact with stream water surfaces and mixing, combined with the use of data from single 'spot' samples collected within a one hour window. It is well recognised that stream contaminant concentrations resulting from single incidents are highly variable on the scale of hours to days (Bruton 1982). It appears, however, that the sampling regime used in this study has been adequate to detect a relationship with buffer strip widths over a broad range of concentrations and conditions.
Atrazine concentrations following the first rain event and one month after spraying were strongly related to those found on the day of spray but not to other site factors. This suggests that contamination of the stream itself or of the immediate riparian area during spraying dictates stream concentrations over the ensuring month and during rain events. The extent of this contamination is apparently dictated by buffer strip width. Thus, the soil erosion class or plantation slope had no significant influence on the stream concentrations after the day of spray.
Contamination of streams draining plantations apparently cannot be completely avoided if triazine herbicides are used. (Davies et al. 1993). From the present study, it would appear that contamination can be minimised by the use of appropriate buffer strips. The maximum buffer strip width examined in this study was 30 m. Median concentrations for all 30 m buffered streams were below 20 ug/L on all occasions following spraying, a concentration below which short term ecological effects are unlikely (Dewey 1986). This was not the case for buffers of 20m or narrower. These results suggest that buffers must be at least 30 m in width in order to minimise the short term ecological impact of atrazine contamination on streams draining sprayed areas. The proposed WHO guideline for atrazine in drinking water, 2 ug/L,was only achieved after one month at sites sprayed with a 30 m buffer.
The results from this study can only be considered as tentative. Ideally, a more intense and stratified sampling program could be used to evaluate the true time pattern of stream concentrations and the mass loss of atrazine from the catchments (Bruton 1982). The present study lacked full representation of buffer strip qualities for each buffer strip width and a detailed investigation of the effects of vegetation density at a range of widths is warranted if either aerial spraying or ground based intensive spraying is maintained as a feature of forestry management.
Davies and Cook (1993) described the impact of a single spraying of cypermethrin on Sales Rivulet. They suggested that mayflies and stoneflies (Ephemeroptera, Plecoptera) were the most sensitive taxa, showing the greatest response in both the drift and benthos. The present study further supports their observations with drift values being highest for these groups at pyrethroid concentrations >0.1 ug/L and having the highest correlation with concentration. It appears that contamination of streams with low concentrations of pyrethroids from spray drift results in significant responses in invertebrate drift which are generally related to the mortality of mayflies and stoneflies (Davies and Cook 1993). In Australia pyrethroid insecticides are widely used in forestry, agriculture and in the cotton industry (Barrett et al. 1991). No Australian studies of their effects have been published to date. In general, they have a short half-life and readily bind to sediments, a behaviour related to their high octanol-water partition coefficients (Vershueren 1983). Thus, effects on stream biota are likely to be restricted to short-term impacts related to practices on the day of spray and not to long-term contamination from runoff. It should be noted, however, that unlike the single application of atrazine per rotation, alphamethrin is frequently applied annually and occasionally more frequently, depending on chrysomelid densities. Repeated short term intensive decreases in invertebrate abundance and/or diversity may have a significant long-term impact on stream ecology.
Given the relative difficulty of obtaining reliable analytical results for trace pyrethroids in the normal field situation, it appears that both ... and ... for invertebrate drift can be used as sensitive short term bioindicators of pyrethroid contamination of streams down to 0.1ug/L. ... values for total fauna and for mayflies and stoneflies in this study were all highly negatively correlated with buffer strip width. A number of authors have reported short term responses in stream invertebrate drift to insecticide contamination on the scale of hours to days (Muirhead-Thompson 1987), including a number of pyrethroids (Kingsbury and Kreutsweiser 1979, Everts et al. 1983), Stephenson (1982) reported 24 h LC50 values for cypermethrin in the range 0.1-0.6 ug/L for a number of invertebrate taxa, including the mayfly Cloeon..
The pyrethoid sprayed plantations examined in this study were drained by streams with buffer strips ranging from 5 to 50 m. All streams drained the sprayed plantations directly. Responses in ... values were observed at all buffer strip widths, with the smallest responses being observed at 50m. It therefore appears that contaimination by pyrethroids is related to buffer strip width and that a strip of at least 50 m is required to minimise that contamination.
Conclusions
Factors affecting spray drift contamination of stream water include
weather conditions, droplet sizes, height of application, density and
quality of plantation and riparian vegetation and buffer strip width.
In this study, contamination of streams immediately following aerial
spraying with atrazine and pyrethroid pesticides was found to be directly
related to the widths of "no-spray" buffer strips. In the case of atrazine,
the magnitude of contamination after the first major rain event and
one month after spraying was directly related to the magnitude on the
day of spray. A marked biological response was observed in the downstream
drift of freshwater invertebrates to contamination by the pyrethroids
alphamethrin and cypermethrin. Recommended minimum buffer strip widths
for minimising contamination in wet sclerophyll forests are 30 m for
atrazine and 50 m for pyrethroids, in conjunction with prescriptive
guidelines for aerial spraying operations (eg Forestry Commission 1988).
HERBICIDE SPILL ALONG RED HILL ROAD, TRARALGON SOUTH - 26 May 1998
- STRZELECKI RANGES.
A spill of Simazine herbicide occurred for about a kilometre along Red Hill Road, finishing near Middle Road. A company crew had been using the material the previous day and had mixed more than they were able to use. When they went to use it they found that the clay particles has settled and had set solidly. They could not clear it so they took the tank back to their workshops to get cleared. It appears that a valve had been left open which had become unblocked on the way down from Balook Road and had leaked.
The leak which was estimated to be about 100 litres and left a white line on the bitumen road surface.
The leak was not reported either to Australian Paper Plantations Pty Ltd or the EPA until several days after the event.
From the EPA Complaint Report:
"Investigated and found bright pink dye on the edge of the road, the slope leading to a waterhole and a pink tinge in the water. Obtained a sample of the waterhole and at the outlet from it."
On 27/5/98 APP was notified and were advised to pump the water out (to be used as make-up water) and to remove the contaminated soil.
Explanation from spray contractors " *** explained that his son ***
had used the suction hose on the new spray unit to pump water into the
spray tank after having put the chemicals and dye into the tank (21
litres simazine, 6 litres roundup, 200 ml pulse and 230 ml dye). When
he had filled the 600 litre tank he stopped the pump and as he took
the hose out of the water he saw the pink liquid running out of the
end of the hose into the water. He quickly threw the hose onto the roadway
and then onto the vehicle. He saw that the water had been coloured with
the dye/chemical mix and that there were stains on the bank and the
road edge. He did not notify anyone because he thought the spill was
too insignificant but he did spread some sawdust on the spill on the
road. It appears that the non-return valve in the hose inlet did not
work when the pump was turned off. They have now installed another non-return
valve in the inlet hose. "
ROUNDUP UPDATES
RoundUp--Lymphoma Connection
From: Sadhbh O' Neill of "Genetic Concern."
PRESS RELEASE - 22 JUNE - New Study Links Monsanto's Roundup to Cancer
A recent study by eminent oncologists Dr. Lennart Hardell and Dr. Mikael Eriksson of Sweden [1], has revealed clear links between one of the world's biggest selling herbicide, glyphosate, to non-Hodgkin's lymphoma, a form of cancer [2].
In the study published in the 15 March 1999 Journal of American Cancer Society, the researchers also maintain that exposure to glyphosate 'yielded increased risks for NHL.' They stress that with the rapidly increasing use of glyphosate since the time the study was carried out, 'glyphosate deserves further epidemiologic studies.'
Glyphosate, commonly known as Roundup, is the world's most widely used herbicide. It is estimated that for 1998, over a 112,000 tonnes of glyphosate was used world-wide. It indiscriminately kills off a wide variety of weeds after application and is primarily used to control annual and perennial plants.
71% of genetically engineered crops planted in 1998 are designed to be resistant to herbicides such as glyphosate, marketed by Monsanto as Roundup. Companies developing herbicide resistant crops are also increasing their production capacity for the herbicides such as glyphosate, and also requesting permits for higher residues of these chemicals in genetically engineered food. For example, Monsanto have already received permits for a threefold increase in herbicide residues on genetically engineered soybeans in Europe and the U.S., up from 6 parts per million (PPM) to 20 PPM.
According to Sadhbh O' Neill of Genetic Concern, 'this study reinforces concerns by environmentalists and health professionals that far from reducing herbicide use, glyphosate resistant crops may result in increased residues to which we as consumers will be exposed in our food.'
'Increased residues of glyphosate and its metabolites are already on sale via genetically engineered soya, common in processed foods. However no studies of the effects of GE soya sprayed with Roundup on health have been carried out either on animals or humans to date,' she continued.
The United States Department of Agriculture (USDA) statistics from 1997 show that expanded plantings of Roundup Ready soybeans (i.e. soybeans genetically engineered to be tolerant to the herbicide) resulted in a 72% increase in the use of glyphosate. According to the Pesticides Action Network, scientists estimate that plants genetically engineered to be herbicide resistant will actually triple the amount of herbicides used. Farmers, knowing that their crop can tolerate or resist being killed off by the herbicides, will tend to use them more liberally.
O' Neill concluded: 'The EPA when authorising Monsanto's field trials for Roundup-ready sugar beet did not consider the issue of glyphosate. They considered this to be the remit of the Pesticides Control Service of the Department of Agriculture. Thus nobody has included the effects of increasing the use of glyphosate in the risk/benefit analysis carried out. It is yet another example of how regulatory authorities supposedly protecting public health have failed to implement the 'precautionary principle' with respect to GMOs.'
ENDS
Further information: Sadhbh O' Neill at 01-4760360 or 087-2258599 or
(home) 01-6774052
Notes
[1] Lennart Hardell, M.D., PhD. Department of Oncology, Orebro Medical Centre, Orebro, Sweden and Miikael Eriksson, M.D., PhD, Department of Oncology, University Hospital, Lund, Sweden, 'A Case-Control Study of Non-Hodgkin Lymphoma and Exposure to Pesticides', Cancer, March 15, 1999/ Volume 85/ Number 6.
The findings are based on a population-based case-control study conducted in Sweden between 1987 - 1990. The necessary data was ascertained by a series of comprehensive questionnaires and follow-up telephone interviews. Dr. Hardell and Dr. Eriksson found that 'exposure to herbicides and fungicides resulted in significantly increased risks for NHL'.
[2] Lymphoma is a form of cancer that afflicts the lymphatic system. It can occur at virtually any part of the body but the initial symptoms are usually seen as swellings around the lymph nodes at the base of the neck. There are basically two main kinds of lymphoma, i.e. Hodgkin's disease and non-Hodgkin's lymphoma.
The incidence of NHL has increased rapidly in most Western countries over the last few decades. According to the American Cancer Society, there has been an alarming 80% increase in incidences of NHL since the early 1970's.
Ingestion of RoundUp has been shown to cause "irritation of the oral mucous membrane and gastrointestinal tract…pulmonary dysfunction, oliguria, metabolic acidosis, hypotension, leukocytosis and fever." Monsanto's own toxicologist, Rebecca Tominack, participated in this study.(Tominack RL, Yang GY, Tsai WJ, Chung HM, Deng JF, 1991. Taiwan National Poison Center survey of glyphosate-surfactant herbicide ingestions. J Toxicol Clin Toxicol 1991; 29 (1): 91-109) Many people report experiencing severe digestive problems related to irritation of their gastrointestinal tract after overexposure to RoundUp, limiting the foods their bodies will tolerate to a very few bland foods.This is believed to be related to the fact that in a 1983 study by Heitanen, Linnainmaa and Vainio, RoundUp's main ingredient, glyphosate, was shown to decrease the hepatic level level of cytochrom P-450, monooxygenase activities, and the intestinal activity of aryl hydrocarbon hydroxylase.The inhibition of erythrocyte glutathione conjugate transport by polyethoxylated surfactants has also been reported in a 1993 letter to FEBS from studies done by P. G. Board, part of the Molecular Genetics Group, John Curtin School of Medical Research, Australian National University, Canberra. Glutathione is a tripeptide which the body produces from the amino acids cysteine, glutamic acid, and glycine. Glutathione is a powerful antioxidant produced in the liver, where it detoxifies harmful compounds so that they can be excreted through the bile. The glutathione released from the liver directly into the bloodstream helps to maintain the integrity of red blood cells and protect white blood cells. Glutathione is also found in the lungs. In the intestinal tract, it is needed for carbohydrate metabolism, and also appears to exert anti-aging effects, aiding in the breakdown of oxidized fats that may contribute to atherosclerosis. Glutathione's role in carbohydrate metabolism is compromised by the effect of RoundUp's surfactant, POEA, on erythrocyte glutathion conjugate transport. RoundUp causes damage to the liver that inhibits the liver's ability to process toxic substances. Research subject animals injected with glyphosate evidenced a depressed function of the liver.
"Glyphosate decreased the hepatic function of cytochrome P-450 and monoxygnease activities and the intestinal activity of aryl hydrocarbon hydrolase." (Heitanen et al, 1983). The P-450 enzyme system is one of the main body systems for detoxifying harmful chemicals. When it becomes impaired by those same chemicals it is supposed to be detoxifying, the effects of a given chemical on the body increase dramatically.(Heitanen, et al., 1983. Effects of phenoxyherbicides and glyphosate on the hepatic and intestinal biotransformation activities in the rat. Acta Pharmacol Toxicol (Copenh) 1983 Aug; 53(2):103-12.) Testing of patients suffering RoundUp overexposure has indicated damage to their P-450 enzyme system.Roundup produces significant increases in sister-chromatid exchanges (SCE), albeit in higher concentrations over those used for other pesticides. This suggests that it should be evaluated in other genetic tests measuring mutations and chromosome aberrations, although few studies of this nature have yet been done.A 1980 study by Vigfusson and Vyse noted sister-chromatid exchanges in human lymphocytes in vitro. This lymphocyte disturbance correlates with the swelling experienced by persons poisoned by RoundUp.
(Vigfusson, N.V. and Vyse, E.R. (1980), "The effect of the pesticides, Dexon, Captan,and Roundup, on sister-chromatid exchanges in human lymphocytes in vitro". MUTATION RESEARCH, v.79 p.53-57.) William Meggs, M.D., Ph.D., School of Medicine, East Carolina University: In patients who have been chemically injured, Meggs has noted significant lymphatic hyperplasia, lymphatic tissue that is swollen and engorged. He has also found significant cobblestoning in upper airway passages. This represents chronic inflammation caused by lymphocytes migrating out of the blood stream and seeping into the tissues. Meggs has also noted thickening of the structure called the basement membrane, the structure on which the lining of cells that lines the interior of the nose sits. Meggs' study also found a defect in the tight junctions (the joining of cells together) and a proliferation of nerve fibers.
"Chemicals bind to receptors on nerve fibers and produce something called neurogenic inflammation. These chemicals bind to these receptors and cause the release of potent substances that produce inflammation in tissue. When chemicals bind to nerve fibers, they can produce inflammation. Inflammation, in turn, produces other changes in the tissue, and it brings in these lymphocytes. We believe that inflammation causes these barrier cells to open up and sometimes even come off the basement membrane. Below the basement membrane is the nerve fibers, so we have a process whereby a chemical exposure will damage the lining of the nose. What happens is people have a large chemical exposure, they breathe in noxious chemicals, and this damages the epithelium. This huge exposure is able to penetrate this barrier we have between the chemicals we breathe in and these nerve cells beneath the lining layer that react to chemicals by producing inflammation. The inflammation, in turn, produces substances that cause further damage to the lining cell, and actually produce the substances which cause the tight junctions between these cells to open up. In some cases the cells actually come off and just leave these bare nerves exposed. Once you have the bare nerves exposed, low levels of chemicals that we all experience every day are enough to produce inflammation which in turn keeps the epithelium damaged.
"RoundUp was found to cause significant DNA damage to erythrocytes (red blood cells) in a study done in 1997 by Clements, Ralph and Petras. RoundUp's surfactant, POEA, is known to cause haemolysis.(Clements C, Ralph S, Pertas M, 1997. Genotoxicity of select herbicides in Rana catesbeiana tadpoles using the alkaline single-cell gel DNA electrophoresis (comet) assay. Environ Mol Mutagen 1997; 29(3):277-288.)(Sawada Y, Nagai Y, Ueyama M, Yamamoto I, 1988. Probable toxicity of surface-active agent in commercial herbicide containing glyphosate. Lancet. 1988 Feb 6;1(8580):299.) In haemolysis, hemoglobin leaks from the red blood cells, leaving them unable to transport sufficient supplies of oxygen to the body's tissues. The chest pains, difficulty breathing, and impaired cognitive skills reported by persons who have sustained RoundUp poisoning also point to impairment of the blood's oxygen transport system, hemoglobin, as being responsible for these symptoms. This impairment of the erythrocytes' ability to deliver adequate oxygen to both brain and body results in impaired tissue perfusion and hypoxia."The brain is particularly vulnerable to hypoxia, and exposure to toxins that interfere with the intake, transport and utilization of oxygen provoke rapid and major neuronal damage. Compounds crossing the blood-brain barrier may induce both general and extremely localized neurotoxic effects."(Kyvik KR, Morn BE, 1995. Environmental poisons and the nervous system. Tidsskr Nor Laegeforen 1995. June 10; 115(15):1834-8.) According to both the EPA and the World Health Organization in 1993 and 1994, glyphosate appears to mimic adrenaline. This would explain the sleeping problems encountered by many persons exposed to RoundUp, as for them, cortisol appears to no longer be properly regulated by their bodies' adrenal glands.(US EPA, 1993. EPA Reregistration Eligibility Document, Glyphosate, Office of Prevention, Pesticides and Toxic Substances, Washington, D.C., September 1993.)(IPCS, 1994. Environmental health criteria 159: Glyphosate. International Programme of Chemical Safety, World Health Organization, Geneva.)
Research on RoundUp's Toxicity
Ingestion of RoundUp has been shown to cause "irritation of the oral mucous membrane and gastrointestinal tract…pulmonary dysfunction, oliguria, metabolic acidosis, hypotension, leukocytosis and fever."
Monsanto's own toxicologist, Rebecca Tominack, participated in this study.
(Tominack RL, Yang GY, Tsai WJ, Chung HM, Deng JF, 1991. Taiwan National Poison Center survey of glyphosate-surfactant herbicide ingestions. J Toxicol Clin Toxicol 1991; 29 (1): 91-109)
Many people report experiencing severe digestive problems related to irritation of their gastrointestinal tract after overexposure to RoundUp, limiting the foods their bodies will tolerate to a very few bland foods.
This is believed to be related to the fact that in a 1983 study by Heitanen, Linnainmaa and Vainio, RoundUp's main ingredient, glyphosate, was shown to decrease the hepatic level level of cytochrom P-450, monooxygenase activities, and the intestinal activity of aryl hydrocarbon hydroxylase.
The inhibition of erythrocyte glutathione conjugate transport by polyethoxylated surfactants has also been reported in a 1993 letter to FEBS from studies done by P. G. Board, part of the Molecular Genetics Group, John Curtin School of Medical Research, Australian National University, Canberra.
Glutathione is a tripeptide which the body produces from the amino acids cysteine, glutamic acid, and glycine. Glutathione is a powerful antioxidant produced in the liver, where it detoxifies harmful compounds so that they can be excreted through the bile. The glutathione released from the liver directly into the bloodstream helps to maintain the integrity of red blood cells and protect white blood cells. Glutathione is also found in the lungs. In the intestinal tract, it is needed for carbohydrate metabolism, and also appears to exert anti-aging effects, aiding in the breakdown of oxidized fats that may contribute to atherosclerosis. Glutathione's role in carbohydrate metabolism is compromised by the effect of RoundUp's surfactant, POEA, on erythrocyte glutathion conjugate transport.
RoundUp causes damage to the liver that inhibits the liver's ability to process toxic substances.
Research subject animals injected with glyphosate evidenced a depressed function of the liver. "Glyphosate decreased the hepatic function of cytochrome P-450 and monoxygnease activities and the intestinal activity of aryl hydrocarbon hydrolase." (Heitanen et al, 1983). The P-450 enzyme system is one of the main body systems for detoxifying harmful chemicals. When it becomes impaired by those same chemicals it is supposed to be detoxifying, the effects of a given chemical on the body increase dramatically.
(Heitanen, et al., 1983. Effects of phenoxyherbicides and glyphosate on the hepatic and intestinal biotransformation activities in the rat. Acta Pharmacol Toxicol (Copenh) 1983 Aug; 53(2):103-12.)
Testing of patients suffering RoundUp overexposure has indicated damage to their P-450 enzyme system.
Roundup produces significant increases in sister-chromatid exchanges (SCE), albeit in higher concentrations over those used for other pesticides. This suggests that it should be evaluated in other genetic tests measuring mutations and chromosome aberrations, although few studies of this nature have yet been done.
A 1980 study by Vigfusson and Vyse noted sister-chromatid exchanges in human lymphocytes in vitro. This lymphocyte disturbance correlates with the swelling experienced by persons poisoned by RoundUp.
(Vigfusson, N.V. and Vyse, E.R. (1980), "The effect of the pesticides, Dexon, Captan, and Roundup, on sister-chromatid exchanges in human lymphocytes in vitro". MUTATION RESEARCH, v.79 p.53-57.)
William Meggs, M.D., Ph.D., School of Medicine, East Carolina University:
In patients who have been chemically injured, Meggs has noted significant lymphatic hyperplasia, lymphatic tissue that is swollen and engorged. He has also found significant cobblestoning in upper airway passages. This represents chronic inflammation caused by lymphocytes migrating out of the blood stream and seeping into the tissues. Meggs has also noted thickening of the structure called the basement membrane, the structure on which the lining of cells that lines the interior of the nose sits. Meggs' study also found a defect in the tight junctions (the joining of cells together) and a proliferation of nerve fibers.
"Chemicals bind to receptors on nerve fibers and produce something called neurogenic inflammation. These chemicals bind to these receptors and cause the release of potent substances that produce inflammation in tissue.
When chemicals bind to nerve fibers, they can produce inflammation. Inflammation, in turn, produces other changes in the tissue, and it brings in these lymphocytes. We believe that inflammation causes these barrier cells to open up and sometimes even come off the basement membrane. Below the basement membrane is the nerve fibers, so we have a process whereby a chemical exposure will damage the lining of the nose.
What happens is people have a large chemical exposure, they breathe in noxious chemicals, and this damages the epithelium. This huge exposure is able to penetrate this barrier we have between the chemicals we breathe in and these nerve cells beneath the lining layer that react to chemicals by producing inflammation. The inflammation, in turn, produces substances that cause further damage to the lining cell, and actually produce the substances which cause the tight junctions between these cells to open up. In some cases the cells actually come off and just leave these bare nerves exposed. Once you have the bare nerves exposed, low levels of chemicals that we all experience every day are enough to produce inflammation which in turn keeps the epithelium damaged."
RoundUp was found to cause significant DNA damage to erythrocytes (red blood cells) in a study done in 1997 by Clements, Ralph and Petras. RoundUp's surfactant, POEA, is known to cause haemolysis.
(Clements C, Ralph S, Pertas M, 1997. Genotoxicity of select herbicides in Rana catesbeiana tadpoles using the alkaline single-cell gel DNA electrophoresis (comet) assay. Environ Mol Mutagen 1997; 29(3):277-288.)
(Sawada Y, Nagai Y, Ueyama M, Yamamoto I, 1988. Probable toxicity of surface-active agent in commercial herbicide containing glyphosate. Lancet. 1988 Feb 6;1(8580):299.)
In haemolysis, hemoglobin leaks from the red blood cells, leaving them unable to transport sufficient supplies of oxygen to the body's tissues.
The chest pains, difficulty breathing, and impaired cognitive skills reported by persons who have sustained RoundUp poisoning also point to impairment of the blood's oxygen transport system, hemoglobin, as being responsible for these symptoms. This impairment of the erythrocytes' ability to deliver adequate oxygen to both brain and body results in impaired tissue perfusion and hypoxia.
"The brain is particularly vulnerable to hypoxia, and exposure to toxins that interfere with the intake, transport and utilization of oxygen provoke rapid and major neuronal damage. Compounds crossing the blood-brain barrier may induce both general and extremely localized neurotoxic effects."
(Kyvik KR, Morn BE, 1995. Environmental poisons and the nervous system. Tidsskr Nor Laegeforen 1995. June 10; 115(15):1834-8.)
According to both the EPA and the World Health Organization in 1993 and 1994, glyphosate appears to mimic adrenaline. This would explain the sleeping problems encountered by many persons exposed to RoundUp, as for them, cortisol appears to no longer be properly regulated by their bodies' adrenal glands.
(US EPA, 1993. EPA Reregistration Eligibility Document, Glyphosate, Office of Prevention, Pesticides and Toxic Substances, Washington, D.C., September 1993.)
(IPCS, 1994. Environmental health criteria 159: Glyphosate. International Programme of Chemical Safety, World Health Organization, Geneva.)
RoundUp and Cholinesterase Inhibition
Monsanto states that glyphosate is not a cholinesterase inhibitor. The MSDS on RoundUp also says that glyphosate is not a cholinesterase inhibitor. Yet, glyphosate is a an organophosphorus, and the "toxic effects of organophosphorus (OP) compounds are predicated on their irreversible inhibition of acetylcholinesterase (AchE) and other serine hydrolases."
(Viragh C, Kovach IM, Pannell L, 1999. Small Molecular Products of Dealkylation in Soman-Inhibited Electric Eel Acetylcholinesterase. American Chemical Society, June 11, 1999.)
Merely saying glyohosate is not a cholinesterase inhibitor, however, does not define whether RoundUp itself in full formulation is a cholinesterase inhibitor, and there are no published studies that purport to answer this question.
In 1988, Yusuke Sawada, et al. did a study in which they concluded that the surfactant in RoundUp (POEA) is more toxic than RoundUp's main ingredient, glyphosate. A study by Servizi et al in 1987 found that POEA is two to three times more toxic than glyphosate, and that the synergy of the two ingredients may even be more acutely toxic than the two ingredients combined.
The answer to whether RoundUp in full formulation is a cholinesterase inhibitor can only be determined by looking at anecdotal evidence. Many doctors, however, based on Monsanto's advertising that glyphosate is not a cholinesterase inhibitor, refuse to test RoundUp poisoning victims for cholinesterase inhibition, so even anecdotal evidence is not readily available.
(Sawada Y, Nagai Y, Ueyama M, Yamamoto I, 1988. Probable toxicity of surface-active agent in commercial herbicide containing glyphosate. Lancet. 1988 Feb 6;1(8580):299.)
(Servizi JA, Gordon RW, Martens DW, 1987. Acute toxicity of Garlon 4 and Roundup herbicides to salmon, Daphnia, and trout. Bull Environ Contam Toxicol. 1987 Jul;39(1):15-22. )
An October 27, 1999 article by PANUPS (Pesticide Action Network Updates Service) offers the information that according to a European Community report on glyphosate (not released at that time), glyphosate poses a significant risk to certain beneficial insects.
(PANUPS, 1999. Glyphosate May Harm Beneficial Organisms, October 27, 1999)
In a 1993 article on organophosphate poisoning, British researcher, T. C. Marrs, indicated that "certain OPs are exploited for their anticholinesterase effects, including defoliants such as 'DEF', herbicides such as glyphosate." The article goes on to say that the cholinergic syndrome is "caused by acetylcholinesterase inhibition."
(Marrs, TC, 1993. Organophosphate poisoning. Pharmacol Ther 1993; 58(1): 51-66.)
An area that has yet to be explored is the impact of the degradation process for glyphosate on the serine cycle. The serine cycle plays a strong part in cholinesterase inhibition in humans. From available research, it is easy to conclude that, while glyphosate itself might not technically be anticholinergic, the degradants of glyphosate might very well be cholinesterase inhibitors.
Glyphosate's degradation pathway shows that, depending one which soil organisms are present, glyphosate degrades into sarcosine, formaldehyde, AMPA, and Methylamine.
Formaldehyde is not only carcinogenic, but impairs the serine cycle, an important part of the human metabolic process. According to a document on the ESTHER database, "cholinesterases are readily phosphorylated at the active site serine by a variety of organophosphorus agents (OP) and carbamates."
(www.ensam.inra.fr/cholinesterase/chem/chemInhibition2.html. The ESTHER "Chemical Mechanism of Acetylcholinesterase Inhibition" introduction.)
(Goldberg I, Mateles RI , 1975. Growth of Pseudomonas C on C1 compounds: enzyme activities in extracts of Pseudomonas C cells grown on methanol, formaldehyde, and formate as sole carbon sources. J Bacteriol 1975 Apr;122(1):47-53)
There is reported evidence of a patient who, after exposures to RoundUp, showed a depressed pseudocholinesterase. SmithKline Beecham's Normal Values reference range is 3200 - 6600. On 6/4/96, after three major exposures to RoundUp, this patient's pseudocholinesterase was 2887. On 7/8/96, after an additional major exposure to RoundUp, this patient's pseudocholinesterase was 2700. The last reading during the period of this patient's exposures to RoundUp was 2733 on 8/7/96. Only with the assistance of successful drug therapy (large doses of dextromethorophan) was this reading reversed to 3586 on 10/22/96.
PANUPS: Monsanto Agrees to Change Ads and EPA Fines Northrup King. January 10, 1997.
Monsanto Agrees to Change Ads and EPA Fines Northrup King Monsanto Co. agreed to change its advertising for glyphosate-based products, including Roundup, in response to complaints by the New York Attorney General's office that the ads were misleading. Based on their investigation, the Attorney General's office felt that the advertising inaccurately portrayed Monsanto's glyphosate-containing products as safe and as not causing any harmful effects to people or the environment. According to the state, the ads also implied that the risks of products such as Roundup are the same as those of the active ingredient, glyphosate, and do not take into account the possible risks associated with the product's inert ingredients.
As part of the agreement, Monsanto will discontinue the use of terms such as "biodegradable" and "environmentally friendly" in all advertising of glyphosate-containing products in New York state and will pay $50,000 toward the state's costs of pursuing the case. The Attorney General has been challenging the ads since 1991.
Monsanto maintains that it did not violate any federal, state or local law and that its claims were "true and not misleading in any way." The company states that they entered into the agreement for settlement purposes only in order to avoid costly litigation.
According to a 1993 report published by the School of Public Health at the University of California, Berkeley, glyphosate was the third most commonly-reported cause of pesticide illness among agricultural workers. Another study from the School of Public Health found that glyphosate was the most commonly reported cause of pesticide illness among landscape maintenance workers. (Both studies were based on data collected between 1984 and 1990.)
In the first nine months of 1996, Monsanto's worldwide agrochemical sales increased by 21% to US$2.48 billion, due largely to increased sales of Roundup.
EPA Fines Northrup King
Also in November 1996, Northrup King Co. agreed to pay a US$165,200 fine to the U.S. Environmental Protection Agency (EPA) for importing, producing, selling and distributing an unregistered pesticide P genetically engineered corn containing Bacillus thurgiensis (Bt). This was EPA's first legal action involving a genetically engineered plant pesticide.
According to EPA, the company's activities violated the U.S. Federal Insecticide, Fungicide and Rodenticide Act and included failing to file with EPA the required paperwork for importing the Bt corn, and producing the pesticide at eight unregistered facilities during 1994-95.
Northrup King, a Sandoz Seeds subsidiary based in Minnesota, maintains that they had been working with the EPA to obtain registration for their Bt corn and expected approval last spring. However, in order to have as much seed as possible to sell to U.S. growers, the company shipped seed to Chile for winter production and brought the increased volumes back to the U.S. for packaging and sale. A company spokesperson stated that the federal process took longer than expected, and therefore Northrup King was in "technical violation" by letting its production get ahead of registration. The originally proposed fine of US$208,500 was reduced by 20% because of what EPA officials called the company's "cooperation and good faith efforts to come into compliance."
Northrup King's Bt corn, developed in collaboration with Monsanto using its Yieldgard technology, was registered on August 5, 1996, and the company has been selling seed to U.S. farmers since then for next season's plantings. According to reports, the company expected to sell out by the end of the 1996, and is projecting 500,000 to one million acres planted with the company's seed by next spring.
Sources: Agrow: World Crop Protection News, November 15, November 29 & December 13, 1996; EPA News Release, Region 5, November 4, 1996; Minneapolis Star Tribune, November 7, 1996; The Gene Exchange, December 1996; Preventing Pesticide-related Illness in California Agriculture, William Pease, et al., 1993; Pesticides in the Home and Community: Health risks and policy alternatives, J.C. Robinson et al., 1994.
Contact: PANNA (see below).
Roundup Inhibits Steroidogenesis by Disrupting Steroidogenic Acute Regulatory (StAR) Protein Expression Lance P. Walsh,1 Chad McCormick,1 Clyde Martin,2 and Douglas M. Stocco1
1Department of Cell Biology and Biochemistry, Texas Tech University
Health Sciences Center, Lubbock, Texas, USA
2Department of Mathematics, Texas Tech University, Lubbock, Texas, USA
Abstract Recent reports demonstrate that many currently used pesticides
have the capacity to disrupt reproductive function in animals. Although
this reproductive dysfunction is typically characterized by alterations
in serum steroid hormone levels, disruptions in spermatogenesis, and
loss of fertility, the mechanisms involved in pesticide-induced infertility
remain unclear. Because testicular Leydig cells play a crucial role
in male reproductive function by producing testosterone, we used the
mouse MA-10 Leydig tumor cell line to study the molecular events involved
in pesticide-induced alterations in steroid hormone biosynthesis. We
previously showed that the organochlorine insecticide lindane and the
organophosphate insecticide Dimethoate directly inhibit steroidogenesis
in Leydig cells by disrupting expression of the steroidogenic acute
regulatory (StAR) protein. StAR protein mediates the rate-limiting and
acutely regulated step in steroidogenesis, the transfer of cholesterol
from the outer to the inner mitochondrial membrane where the cytochrome
P450 side chain cleavage (P450scc) enzyme initiates the synthesis of
all steroid hormones. In the present study, we screened eight currently
used pesticide formulations for their ability to inhibit steroidogenesis,
concentrating on their effects on StAR expression in MA-10 cells. In
addition, we determined the effects of these compounds on the levels
and activities of the P450scc enzyme (which converts cholesterol to
pregnenolone) and the 3ß-hydroxysteroid dehydrogenase (3ß-HSD) enzyme
(which converts pregnenolone to progesterone). Of the pesticides screened,
only the pesticide Roundup inhibited dibutyryl [(Bu)2]cAMP-stimulated
progesterone production in MA-10 cells without causing cellular toxicity.
Roundup inhibited steroidogenesis by disrupting StAR protein expression,
further demonstrating the susceptibility of StAR to environmental pollutants.
Key words: chemical mixtures, cytochrome P450 side chain cleavage, environmental
endocrine disruptor, 3ß-hydroxysteroid dehydrogenase, Leydig cells,
Roundup, steroid hormones, steroidogenesis, steroidogenic acute regulatory
protein. Environ Health Perspect 108:769-776 (2000).
[Online 12 July 2000]
http://ehpnet1.niehs.nih.gov/docs/2000/108p769-776walsh/abstract.html
Address correspondence to D.M. Stocco, Department of Cell Biology and Biochemistry, Texas Tech University Health Sciences Center, Lubbock, TX 79409 USA. Telephone: (806) 743-2505. Fax: (806) 743-2990. E-mail: doug.stocco@ttmc.ttuhsc.edu We thank D. Alberts for technical assistance.
This work was supported by NIH grant HD17481 to D. Stucco. L. Walsh was supported by NIH grant T32-HD07271 and a scholarship from the Lubbock Achievement Awards for College Scientists Chapter.
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