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This area should give more information on TPP and OrganioPhosphates in general. This includes the signs and symptoms and other ways of exposure

The following quote is taken from a study on

Organophosphate-based pesticides and genetic damage implicated with bladder cancer.

Authored by

Helen Moriarty, Lucy Webster, Geoff McKenzie, John Kent

School of Biomedical Sciences, Faculty of Health Studies

Charles Sturt University

 

They say that :

"Organophosphate-based pesticides have been associated with pathology and chromosomal damage in humans. There are also epidemiological links between organophosphate-based pesticides and cancer. Currently low-level chemical exposure receives less attention than does acute poisoning and the few screening tests for low level occupational exposure are of doubtful sensitivity. This investigation evaluated four methods and undertook a pilot study of safe-handling practices among a group of workers with occupational exposure to organophosphate-based pesticides in the Riverina area, Australia. Blood samples were studied from ten farmers before and after occupational exposure to the pesticides and from five unexposed controls."

bulletFurther they concluded

"that Howell-Jolly body and chromosome breakage analysis are sensitive indicators of cell nuclear damage resulting from low level occupational exposure to organophosphates. Such nuclear damage could be implicated in carcinogenesis; the development of bladder cancer is one such example.

In addition, it was found that despite the education of 70% of the farmers tested, not one of them abided by all of the safety procedures recommended. The design of protective clothing may need to be reevaluated in order to increase compliance."

bulletThe excellent introduction to their study is included here as it speaks of organophosphate chemicals in general. Though their concern is with insecticides but from our point of view it is another indicator of the contention that the general level of exposure in the community is far greater than is generally recognized. Therefore I would contend that the danger from the eluted emissions from computer monitors when taken together with other sources of exposure may be far greater than recognized to date.

Introduction

The organophosphate-based chemicals act as anti-cholinesterase substances and are widely used throughout the world (1). Organophosphate-based chemicals are most commonly insecticides but they are also used in fungicides and herbicides, and have common usage in agriculture. Specifically, they have been used to control insect numbers in commercial crops, as well as to control parasites on animals such as sheep and cattle (eg. fly-strike control). One significant advantage organophosphate chemicals offer over other insecticide agents such as organochlorines (eg. DDT) is that they are much less persistent in the environment (2). Despite the advantages the application of these pesticides has to offer, there is also the potential for considerable adverse affects to those exposed over extended periods of time (2).

A variety of short term and chronic effects may be experienced following repeated or prolonged exposure to organophosphate-based pesticide exposure including difficulty in breathing, involuntary muscle contractions, blurred vision, tear formation, bleeding in the eye, nausea, headache, confusion and slurred speech (1, 3). Little information has been gathered with respect to long term effects of sublethal doses over a period of time but reports

of depression, memory loss and chronic fatigue syndrome have been presented (1, 3, 4); there is also evidence of a possible carcinogenic effect of organophosphate-based pesticides (5, 6).

Considerable attention has been given to the indicators of genetic damage such as chromosomal aberrations, sister-chromatid exchanges and micronuclei to observe human populations occupationally exposed to organophosphate-based pesticides (5, 7, 8, 9). The precise effects of these chromosomal aberrations induced by occupational exposure to organophosphate-based pesticides are not fully known, but the increase in the number of these aberrations following exposure suggests an increase in the likelihood of cancer development induced by chromosomal damage (6, 8, 10).

There are 118 locations in human chromosomes that have been recognised as having a susceptibility to breakage and these are known as fragile sites. These sites can be observed in the laboratory as chromosomal breaks and gaps following the application of particular chemicals. The number of sites expressed varies between individuals and they show a Mendelian pattern of inheritance. Chromosome breakage is a common occurrence and is usually repaired before cell division proceeds.

The scoring of fragile sites can detect exposure to DNA damaging agents (clastogens) such as X-rays and certain chemicals such as nitrogen mustard or diepoxybutane because the number of fragile sites can be increased in these situations. An even more sensitive test can be obtained when a recognised chromosomal damaging agent is applied in the laboratory to blood samples collected from subjects who have been suspected of being environmentally exposed to a DNA damaging agent. Even mild exposure to clastogenic agents can be detected with this method (11)..

Aphidicolin is the usual inducing agent employed for environmental studies (11, 13, 14, 15, 16); in this context it can induce 67% of the recognised fragile sites in the human genome (12). In 1995 Sbrana and Musio (11) reported an increase in the expression of aphidicolin induced chromosomal fragile sites following occupational exposure to pesticides. This observation reinforced the existence of a link between exposure to clastogenic agents (eg. organophosphate-based pesticides) and fragile site induction. Furthermore, the analysis of the breakage effects of different carcinogens on fragile site regions appeared to be significant in the carcinogenic process of many cancers. Enhanced expression of particular fragile sites were implicated in cancers such as the leukaemias, and non-Hodgkin’s lymphoma and those sites were also the locations of numerous tumour suppressor genes and oncogenes (11, 16). These authors also reported that fragile site expression was a reproducible cell response to human exposure to pesticides (16).

Farmers are one occupational group with a high usage of organophosphate-based pesticides, and thus form a group of potential high risk to the types of genetic damage described above. In this connection, a number of studies have shown an increase in cancer incidence of numerous tumour types among the farming population. These included: bladder cancer (17, 18), prostate cancer (17, 19, 20, 21), non-Hodgkin’s lymphoma (19, 20, 22), multiple myeloma (19, 20), skin cancer (20, 23) kidney cancer (17) and lung cancer (23). Our group looked particularly at bladder cancer, because there is a greater incidence of this type of cancer in our area, the Riverina (6th most common in males) compared to the state of New South Wales in general (8th most common in males) (24)."

 

 

 

bulletAdded to the above is the following material which is based on the work of Winder & Balouet of the University of New South Wales in 2001. They were investigating effects on cabin crew of aircraft exposed to oil fumes containg TriCresyl Phosphate.

"Toxicology of the Organophosphates

Human toxicity to organophosphorus compound has been known since 1899, when neurotoxicity to to phospho-creosole (then used in the treatment of tuberculosis) was reported. The study of the toxicity is extensive with two very well established mechanisms on esterases and on neurotoxic esterases(NTE)"

Most commonly and critically affected is the neurotransmitter acetylcholine.. Any organ or tissue which receives this increased output will become increasingly active. This mechanism produces the majority of the symptoms of this poisoning.

The signs include headache, dizziness, general weakness, lethargy, drowsiness, difficulty in concentration, slurred speech, instability and hypothermia.. Early symptoms of poisoning are watering of the eyes, vision problems, overproduction of saliva, nausea and vomiting, abdominal pains and cramps, twitching of muscles, irregular hear beat and circulation problems. All of these things are the result of overproduction of acetylcholine.

Continued damage can lead to a condition which is called what is called Organo-Phosphorus Induced Delayed Neuropathy (OPIDN). Winder & Balouet state that this mechanism is now well understood. And also in regard to OPIDN that "humans are considered to be among the most sensitive species." The mechanism involved is when the organo-phosphate(OP) molecules bind to the long part of the nerve called the Axon and cause disruption to the food supply to the nerve. The axon becomes swollen. Damage can then occur to the end of the axon where the nerve impulses are transmitted. There can then also be deterioration of the insulation surrounding the nerves. Lower limbs which have the longest nerves are most senstive due to their greater need for nutrition, followed by the arms and hands. Tingling is felt, burning,sensation, weakness, tremor in severe cases paralysis.

More recently chronic exposure has evidenced neuro-psychological effects and has been named COPIND Symptoms include Headache, mental fatigue, depression, anxiety, irritability. Reduced concentration and vigilance. Decreased information processing and psychomotor speed. Memory problems and linguistic disturbances. These symptoms can be associated with short term exposure or long term low level repeated exposure. "It is also not known if these symptoms are permanent"(Winder & Balouet)

 

 

 

 
 
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