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Some Studies on Pesticides
Pollution, and Toxins

Home ||| Research Menu Page ||| Last update 12/31/2012

In reverse date order:

Lanphear 2012 Attention-Deficit/Hyperactivity Disorder: A Preventable Epidemic?
Rathee 2012 Bisphenol A in dental sealants and its estrogen like effect.
Andersen 2010Chronic obstructive pulmonary disease and long-term exposure to traffic-related air pollution: a cohort study.
Bouchard 2010Attention-deficit/hyperactivity disorder and urinary metabolites of organophosphate pesticides.
Sagiv 2010Prenatal organochlorine exposure and behaviors associated with attention deficit hyperactivity disorder in school-aged children.
Eskenazi 2007Organophosphate Pesticide Exposure and Neurodevelopment in Young Mexican-American Children.
Labie 2007Developmental neurotoxicity of industrial chemicals.
Ribas-Fito 2007Exposure to hexachlorobenzene during pregnancy and children's social behavior at 4 years of age.
Lu 2006Organic Diets Significantly Lower Children's Dietary Exposure to Organophosphorus Pesticides.
Braun 2006Exposures to Environmental Toxicants and Attention Deficit Hyperactivity Disorder in U.S. Children
Bouma 2002Migration of phthalates from PVC toys into saliva simulant by dynamic extraction.
Dorner 2002DDT in human milk and mental capacities in children at school age: an additional view on PISA 2000.
Garry 2002Birth Defects, Season of Conception, and Sex of Children Born to Pesticide Applicators Living in the Red River Valley of Minnesota, USA.
Schettler 2001Toxic threats to neurologic development of children.
Watanabe 2001Selenium deficiency and brain functions: the significance for methylmercury toxicity
Tirado 2000Pneuropsychological disorders after occupational exposure to mercury vapors in El Bagre (Antioquia, Colombia)
Bazylewicz 1999Behavioral effects of occupational exposure to organophosphorous pesticides in female greenhouse planting workers.
Takayams 1999Effects of long-term oral administration of DDT on nonhuman primates.
Baldi 1998Delayed health effects of pesticides: review of current epidemiological knowledge
Dencker 1998Susceptibility in utero and upon neonatal exposure.
Hauser 1998Resistance to thyroid hormone: implications for neurodevelopmental research on the effects of thyroid hormone disruptors.
Kurt 1998Epidemiological association in US veterans between Gulf War illness and exposures to anticholinesterases.
MMWR 1998Lead poisoning associated with imported candy and powdered food coloring--California and Michigan.
Sonnenschein 1998An updated review of environmental estrogen and androgen mimics and antagonists.
Weiss 1998A risk assessment perspective on the neurobehavioral toxicity of endocrine disruptors.
Acuna 1997Assessment of neurotoxic effects of methyl bromide in exposed workers.
Jamal 1997Neurological syndromes of organophosphorus compounds.
Ross 1997Changes in operant behavior of rats exposed to lead at the accepted no-effect level.
Rossi 1997Prenatal exposure to methylmercury alters locomotor activity of male but not female rats.
De Salvia 1995Irreversible impairment of active avoidance behavior in rats prenatally exposed to mild concentrations of carbon monoxide.
Johns 1995Prenatal cocaine exposure affects social behavior in Sprague-Dawley rats.
Kishi 1995Effect of prenatal exposure to styrene on the neurobehavioral development, activity, motor coordination, and learning behavior of rats.
Lindstrom 1995Workshop on perinatal exposure to dioxin-like compounds. I. Summary.
Raby 1995The Examination of the Link Between Pesticides in Food and Learning Disorders in Children.
Cherry 1993Neurobehavioural effects of solvents: the role of alcohol.
Janicke 1993The effects of prenatal alcohol exposure on the behavior of rats during their life span.
Landrigan 1993Strategies for the prevention of environmental neurotoxic illness.
Cooke 1991The health effects of aluminium--a review.
Selvin 1991Chronic lead exposure induces alterations on local circuit neurons.
Cagiano 1990Evidence that exposure to methyl mercury during gestation induces behavioral and neurochemical changes in offspring of rats.
Goyer 1990Lead toxicity: from overt to subclinical to subtle health effects.
Burright 1989Postpartum aggression and plasma prolactin levels in mice exposed to lead.
Chen 1989The effects of inhalation of styrene on the neurobehavior in the offsprings
Dumont 1989Psychotoxicology: the return of the mad hatter.
Weiss 1988Behavior as an early indicator of pesticide toxicity.
Cawte 1985Psychiatric sequelae of manganese exposure in the adult, foetal and neonatal nervous systems.
Ruppert 1985Development of locomotor activity of rat pups exposed to heavy metals.
Nelson 1984Behavioral and neurochemical alterations in the offspring of rats after maternal or paternal inhalation exposure to the industrial solvent 2-methoxyethanol.
Chandra 1983Psychiatric illness due to manganese poisoning.
Fernandez 1983Effects of chronic alcohol exposure on offspring activity in rats.
Lorenzana 1983Neonatal effects of toluene on the locomotor behavioral development of the rat.
McBride 1982Blood lead levels and behaviour of 400 preschool children.
Yamawaki 1982Effects of toluene inhalation on locomotor activity and brain catecholamine levels in rats.
Gross 1981Changes in operant behavior of rats exposed to lead at the accepted no-effect level.
Fechter 1980Prenatal carbon monoxide exposure alters behavioral development.
Tilson 1980Postnatal exposure to benzene alters the neurobehavioral functioning of rats when tested during adulthood.

Selected Environmental Research Foundation Articles on Toxins

  1. ADHD and Children's Environment 1999
  2. Another Pesticide Surprise 1998
  3. Chemicals and the Brain, Part 1 1996
  4. Chemicals and the Brain, Part 2 1996
  5. Drugs In The Water 1998
  6. Ethical Hazards of Risk Assessment 1996
  7. Hazardous Waste Is Legally 'Recycled' Into Pesticides And Labeled 'Inert' 1991
  8. Missing Boys 1998
  9. National Academy Study Says Superfund Dumps Cause Many Illnesses In Humans 1992
  10. New Mechanism Of Disease 1998
  11. Our Stolen Future, Part 1 1996
  12. PCB Exposure Linked to Low IQ 1996
  13. Pesticides and Aggression 1999
  14. Pesticides in the News 1999
  15. Preferring the Least Harmful Way 2000

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  1. Assessment of neurotoxic effects of methyl bromide in exposed workers Acuna MC, Diaz V, Tapia R, Cumsille MA, Rev Med Chil 1997 Jan;125(1):36-42
    "Methyl bromide is ... a pesticide that causes skin, kidney, respiratory, liver and neurological damage. ... Symptoms that appeared with a higher frequency in exposed workers were insomnia, headache, paresthesiae, mood changes and loss of memory and concentration. ... CONCLUSIONS: Acute and chronic methyl bromide exposure causes important psychological and neurological derangement.
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  2. Chronic Obstructive Pulmonary Disease and Long-Term Exposure to Traffic-Related Air Pollution: A Cohort Study. Andersen ZJ, Hvidberg M, Jensen SS, Ketzel M, Loft S, Sřrensen M, Tjřnneland A, Overvad K, Raaschou-Nielsen O, American Journal of Respiratory and Critical Care Medicine, 2010 Sep 24. [Epub ahead of print]
    "Short-term exposure to air pollution has been associated with exacerbation of chronic obstructive respiratory disease (COPD) whereas the role of long-term exposures on the development of COPD is not yet fully understood. ... We followed 57 053 participants in the Danish Diet, Cancer and Health cohort in the Hospital Discharge Register for their first hospital admission for COPD between 1993 and 2006. We estimated the annual mean levels of nitrogen dioxide (NO2) and nitrogen oxides (NOx) at all residential addresses of the cohort participants since 1971 ... CONCLUSIONS: Long-term exposure to traffic related air pollution may contribute to the development of COPD with possibly enhanced susceptibility in people with diabetes and asthma."
    Full Text of Study - Get Password
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  3. Delayed health effects of pesticides: review of current epidemiological knowledge Baldi I, Mohammed-Brahim B, Brochard P, Dartigues JF, Salamon R., Rev Epidemiol Sante Publique 1998 Mar;46(2):134-42
    "...The use of pesticides has extensively grown in the last decades, regardless of the economic level of the countries. ... long term effects are not properly assessed. ... Epidemiologic studies on pesticides have found associations with long-term effects on health mainly in three fields: cancer (especially hematological cancer), neurotoxic effects (polyneuropathy, neuro-behavioral hazards, Parkinson's disease), and reproductive disorders (infertility, birth defects, adverse pregnancy outcomes, perinatal mortality). ... But the continuous development of pesticide use in agriculture, and also in domestic environment, emphasizes the need for epidemiologic studies on long-term effects of pesticides relying on accurate exposure assessment."
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  4. Behavioral effects of occupational exposure to organophosphorous pesticides in female greenhouse planting workers. Bazylewicz-Walczak B, Majczakowa W, Szymczak M, Neurotoxicology 1999 Oct;20(5):819-26
    "51 women employed in gardening enterprises were studied... The comparison group consisted of 25 women not exposed to neurotoxic chemicals... The level of total exposure in the planting worker group was low. ... The exposed female workers were characterized by longer reaction times and reduced motor steadiness compared to the unexposed workers. In addition, increased tension, greater depression and fatigue, more frequent symptoms of CNS disturbances were observed in the exposed women compared to the controls."
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  5. Attention-deficit/hyperactivity disorder and urinary metabolites of organophosphate pesticides. Bouchard MF, Bellinger DC, Wright RO, Weisskopf MG. Pediatrics. 2010 Jun;125(6):e1270-7. Epub 2010 May 17.
    "...Cross-sectional data from the National Health and Nutrition Examination Survey (2000-2004) were available for 1139 children, who were representative of the general US population. ... RESULTS: One hundred nineteen children met the diagnostic criteria for ADHD. Children with higher urinary dialkyl phosphate concentrations, especially dimethyl alkylphosphate (DMAP) concentrations, were more likely to be diagnosed as having ADHD. . . For the most-commonly detected DMAP metabolite, dimethyl thiophosphate, children with levels higher than the median of detectable concentrations had twice the odds of ADHD ... compared with children with undetectable levels. CONCLUSIONS: These findings support the hypothesis that organophosphate exposure, at levels common among US children, may contribute to ADHD prevalence. . ."
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  6. Migration of phthalates from PVC toys into saliva simulant by dynamic extraction. Bouma K, Schakel DJ. Food Addit Contam. 2002 Jun;19(6):602-10.
    " Soft PVC children's products are usually plasticized with phthalates. As young children suck and chew on toys, they extract and ingest certain quantities of the plasticizers. Some phthalates are suspected to affect the kidneys and liver and cause testicular damage. . . Substitutes found for phthalates plasticizers are acetyltributylcitrate, tributylcitrate and diisononyladipate. . . The toxicity and the migration behaviour of these substances is less known and requires more attention. To ensure the safety of PVC toys, these substances should also be regulated. "
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  7. Exposures to environmental toxicants and attention deficit hyperactivity disorder in U.S. children. Braun JM, Kahn RS, Froehlich T, Auinger P, Lanphear BP. Environmental Health Perspectives, 114(12), 1904-9
    " ... these data suggest that prenatal tobacco exposure accounts for 270,000 excess cases of ADHD, and lead exposure accounts for 290,000 excess cases of ADHD in U.S. children. We conclude that exposure to prenatal tobacco and environmental lead are risk factors for ADHD in U.S. children. "
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  8. Postpartum aggression and plasma prolactin levels in mice exposed to lead. Burright RG, Engellenner WJ, Donovick PJ, Physiol Behav 1989 Nov;46(5):889-93
    " Young-adult, female Binghamton Heterogeneous Stock (HET) mice either were exposed to lead via drinking water from birth, or not. Eight days after giving birth to their first litter of pups ... postpartum aggression tests were conducted. Unfamiliar Het male intruders were introduced to the primiparous dams' nesting cages... Behaviorally, the intensity of fighting was greater in lead-exposed pairs than in water-control pairs that fought. ... Plasma prolactin levels implied that lead exposure alone decreased circulating prolactin in primiparous Het dams eight days postpartum, but confrontation with a male intruder also was sufficient to reduce prolactin levels in water-control dams... The data suggest that lead ingestion may... modify: 1) neurotransmitter and hormonal systems and 2) social behavior. The major effect of "subclinical" lead toxicity may be to change the limits of an organism's ability to cope with its environment. "
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  9. Evidence that exposure to methyl mercury during gestation induces behavioral and neurochemical changes in offspring of rats. Cagiano R, et al., Neurotoxicol Teratol 1990 Jan-Feb;12(1):23-8
    "... evidence that acute MMC exposure during prenatal life might induce permanent disturbances in learning and memory which could be partially related to a reduced functional activity of the glutamatergic system is provided."
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  10. Psychiatric sequelae of manganese exposure in the adult, foetal and neonatal nervous systems. Cawte J, Aust N Z J Psychiatry 1985 Sep;19(3):211-7
    "It is important for psychiatrists to recognise that vulnerability to the trace element manganese is different in the adult, foetal and neonatal nervous systems, and that different syndromes may result from exposure."
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  11. Psychiatric illness due to manganese poisoning. Chandra SV, Acta Psychiatr Scand Suppl 1983;303:49-54
    "...Manganese produced hyperactivation [in rats] after 14 and 30 days ... increase in fighting score were also observed after 30 days. These behavioral changes were associated with increased levels of striatal dopamine and norepinephrine in rats exposed to manganese. ..."

    Note: Soy formula for babies has much more manganese than breast milk, and some of children in trouble with the law in their early teens have been found to still have elevated levels of manganese.

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  12. The effects of inhalation of styrene on the neurobehavior in the offsprings Chen BQ, Chung Hua Yu Fang I Hsueh Tsa Chih 1989 Nov;23(6):342-5
    "...Even exposure to relatively low concentrations of styrene delayed some physiological developments, in addition to causing disturbances of the neuromotor coordination function ... and learning acquisition.... large dose led to subtle changes in emotional behavior and increases in spontaneous activities in addition to the delay of neurobehavioral developments."
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  13. Neurobehavioural effects of solvents: the role of alcohol. Cherry N, Environ Res 1993 Jul;62(1):155-8
    "...Results from three recent studies suggest that solvent-exposed workers are particularly at risk of disabling psychiatric illness associated with alcoholism. ... exposure to one substance might potentiate the effect of the other. Concurrent exposure to alcohol and solvents slows clearance of the solvent and might be expected to prolong internal exposure to the neurotoxin. ... it appears that the interrelation between the two exposures may be more important than previously suspected."
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  14. The health effects of aluminium--a review. Cooke K, Gould MH, J R Soc Health 1991 Oct;111(5):163-8
    "This review covers the occurrence of aluminium in soil, air, water and food. In addition, aluminium levels in body tissues and its movement within the body have been considered. The adverse effects of aluminium that have been reported in recent years include Alzheimer's disease, dementia and hyperactivity and learning disorders in children."
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  15. Susceptibility in utero and upon neonatal exposure. Dencker L, Eriksson P, Food Addit Contam 1998;15 Suppl:37-43
    "...For the postnatal period, some neurotoxic pesticides and environmental pollutants, known to affect adult behaviour in experimental animals after perinatal [around birth time] exposure, are given as examples."
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  16. Irreversible impairment of active avoidance behavior in rats prenatally exposed to mild concentrations of carbon monoxide. De Salvia MA, et al., Psychopharmacology (Berl) 1995 Nov;122(1):66-71
    "... gestational exposure to [mild levels of Carbon Monoxide] CO induces in rat offspring permanent learning and memory impairment, confirm that the offspring of smoking mothers may be at considerably greater risk than current epidemiological studies on birthweight and neonatal mortality suggest."
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  17. DDT in human milk and mental capacities in children at school age: an additional view on PISA 2000 De Salvia MA, et al., Psychopharmacology (Berl) 1995 Nov;122(1):66-71
    "OBJECTIVES: To investigate a possible lasting impact of dichlorodiphenyl trichloroethane (DDT) exposure in neonatal life on mental capacities in later life. . . CONCLUSIONS: These data in association with additional experimental and epidemiological findings suggest that DDT is a "neuroendocrine disrupter" as well as a "functional teratogen" leading to harmful effects on brain development and mental capacities in later life. . ."
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  18. Psychotoxicology: the return of the mad hatter. Dumont MP, Soc Sci Med 1989;29(9):1077-82
    "...Psychiatrists have not been attentive to the huge and expanding capacity of neurotoxic substances to induce symptoms of emotional and behavioral dysfunction. ... Psychiatrists should routinely inquire about exposure to toxic substances. ..."
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  19. Organophosphate pesticide exposure and neurodevelopment in young Mexican-American children. Eskenazi B, Marks AR, Bradman A, Harley K, Barr DB, Johnson C, Morga N, Jewell NP. Environmental Health Perspectives. 2007 May;115(5):792-8. Epub 2007 Jan 4.
    "BACKGROUND: Organophosphate (OP) pesticides are widely used in agriculture and homes. Animal studies suggest that even moderate doses are neurodevelopmental toxicants, but there are few studies in humans. OBJECTIVES: We investigated the relationship of prenatal and child OP urinary metabolite levels with children's neurodevelopment. . . CONCLUSIONS: We report adverse associations of prenatal DAPs [dialkylphosphate metabolites] with mental development and pervasive developmental problems at 24 months of age. . ."
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  20. Prenatal carbon monoxide exposure alters behavioral development. Fechter LD, Annau Z, Neurobehav Toxicol 1980 Spring;2(1):7-11
    "The potential for mild prenatal carbon monoxide (CO) exposure by means of maternal cigarette smoking or industrial and ambient air sources is extremely high, but the biological consequences and, in particular, the neurobehavioral effects are undetermined. ... The results .. indicate that such exposure has significant functional consequences for the developing rat."
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  21. Effects of chronic alcohol exposure on offspring activity in rats. Fernandez K, Caul WF, Osborne GL, Henderson GI, Neurobehav Toxicol Teratol 1983 Jan-Feb;5(1):135-7
    "... At adulthood, the treated offspring ambulated [walked around] more than the non-treated offspring in an open field and made a higher number of entrances into a shocked area between trials ... These behavioral results are consistent with findings of increased open field activity and impaired ability to inhibit responding reported by other investigators in rats after prenatal alcohol administration."
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  22. Birth Defects, Season of Conception, and Sex of Children Born to Pesticide Applicators Living in the Red River Valley of Minnesota, USA. Garry VF, Harkins ME, Erickson LL, Long-Simpson LK, Holland SE, Burroughs BL. Environmental Health Perspectives, 2002 Jun;110 Suppl 3:441-9.
    " ... these studies point out that (a) herbicides applied in the spring may be a factor in the birth defects observed and (b) fungicides can be a significant factor in the determination of sex of the children of the families of the RRV. Thus, two distinct classes of pesticides seem to have adverse effects on different reproductive outcomes. Biologically based confirmatory studies are needed."
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  23. Lead toxicity: from overt to subclinical to subtle health effects. Goyer RA, Environ Health Perspect 1990 Jun;86:177-81
    " Although the toxicity of lead was recognized centuries ago, concern was restricted to overt symptoms: colic, encephalopathy, anemia, or renal disease. ... Identification of subclinical effects has been possible the last 15 or 20 years because of the development of sensitive measures to detect cognitive and behavioral changes that are not apparent clinically and because of methods to measure the reduced activity of heme enzymes. ... The new awareness prompted ..the establishment of maximum recommended exposures in children to a blood lead level of 25 micrograms/dL. ... Current research implicates lead as a contributing etiologic factor in a number of common diseases affecting large portions of the population such as subtle cognitive and neurological deficits, hypertension, congenital malformations, immunotoxicity, and deficits in growth and development. ..."
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  24. Changes in operant behavior of rats exposed to lead at the accepted no-effect level. Gross-Selbeck E, Gross-Selbeck M, Clin Toxicol 1981 Nov;18(11):1247-56
    "After weaning, male and female Wistar rats were fed a daily diet containing 1 g lead acetate/kg food until a level of about 20 micrograms/100 mL blood was obtained. The male rats were subjected to the different behavioral tests, whereas the females were mated to untreated males and further exposed until weaning of the offspring. ... the rats exposed to lead after weaning showed slight changes of DRH performance. By contrast, in pre- and neonatally exposed animals, DRH performance was significantly increased, although blood-lead levels had returned to normal at the time of testing. A comparison of lead effects in animals to possible effects in man is discussed in this paper, and it is concluded that lead exposure to man at doses which presently are suggested to be innocuous [harmless] may result in subclinical functional changes of the central nervous system."
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  25. Resistance to thyroid hormone: implications for neurodevelopmental research on the effects of thyroid hormone disruptors. Hauser P, McMillin JM, Bhatara VS, Toxicol Ind Health 1998 Jan-Apr;14(1-2):85-101
    "Thyroid hormones are essential for normal behavioral, intellectual, and neurological development. Congenital hypothyroidism, if not treated, can result in irreversible mental retardation, whereas thyroid diseases with more moderate impairment of thyroid function, such as resistance to thyroid hormone, cause less severe intellectual and behavioral abnormalities, including attention deficit hyperactivity disorder. There is increasing evidence that exposure to certain synthetic compounds, including dioxins and polychlorinated biphenyls (PCBs), during the perinatal period can also impair learning, memory, and attentional processes in offspring. Animal and human studies suggest that exposure to these environmental toxicants impair normal thyroid function. ... Such studies may provide new insights into the basic pathogenesis of developmental neurotoxicity following exposure to thyroid-disrupting synthetic compounds.
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  26. Neurological syndromes of organophosphorus compounds. Jamal GA, Adverse Drug React Toxicol Rev 1997 Aug;16(3):133-70
    "...In addition to the acute cholinergic poisoning, organophosphorus (OP) compounds are capable of producing several subacute, delayed and chronic neurological, neurobehavioural and psychiatric syndromes. ... New concepts in neurotoxicology are being produced from recent studies which may necessitate a new radical approach to the assessment of neurotoxicity of pesticides before releasing them for widespread use."
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  27. The effects of prenatal alcohol exposure on the behavior of rats during their life span. Janicke B, Coper H, J Gerontol 1993 Jul;48(4):B156-67
    "... In the juvenile phase ... no substantial differences ... Exceptions ...transiently higher exploratory activity in the open field test. In the adult phase ... reduced performance was observed in basic functions such as body temperature regulation. ... During the senile phase .. impairment of nearly all tested functions occurred earlier and was more pronounced."
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  28. Prenatal cocaine exposure affects social behavior in Sprague-Dawley rats. Johns JM, Noonan LR, Neurotoxicol Teratol 1995 Sep-Oct;17(5):569-76
    "Children prenatally exposed to cocaine are reported to exhibit inappropriate social behavior, including aggression. ... Our data indicate that prenatal cocaine treatment in rats increases fear or aggression responses, dependent on sex and stimulus situation."
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  29. Effect of prenatal exposure to styrene on the neurobehavioral development, activity, motor coordination, and learning behavior of rats. Kishi R, Chen BQ, Katakura Y, Ikeda T, Miyake H, Neurotoxicol Teratol 1995 Mar-Apr;17(2):121-30
    "Maternal Wistar rats were exposed via inhalation to 0, 50, or 300 ppm styrene for 6 h/day during gestation ... Exposure to low concentrations of styrene (50 ppm) caused disturbances in motor coordination in addition to delaying some motor and reflex developments. Large doses (300 ppm) led to changes in open-field behavior and increases in spontaneous activity in addition to the delay in neurobehavioral developments..."
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  30. Epidemiological association in US veterans between Gulf War illness and exposures to anticholinesterases. Kurt TL, Toxicol Lett 1998 Dec 28;102-103:523-6
    "To investigate complaints of Gulf War veterans, epidemiologic, case-control and animal modeling studies were performed.... Auditory evoked potentials showed dysfunction, ... nystagmic velocity on rotation testing, .... Brain dysfunction was shown on the Halstead Impairment Index ... These investigations lend credibility that sublethal exposures to drug-chemical combinations caused delayed-onset neurotoxic variants."
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  31. Developmental neurotoxicity of industrial chemicals. Labie D., Medecine Sciences (Paris). 2007 Oct;23(10):868-72.
    "A Silent Pandemic : Industrial Chemicals Are Impairing the Brain Development of Children Worldwide. Fetal and early childhood exposures to industrial chemicals in the environment can damage the developing brain and can lead to neurodevelopmental disorders (NDDs)--autism, attention deficit disorder (ADHD), and mental retardation. In a new review study, published in The Lancet, Philip Grandjean and Philip Landrigan from the Harvard School of Public Health systematically examined publicly available data on chemical toxicity in order to identify the industrial chemicals that are the most likely to damage the developing brain. The researchers found that 202 industrial chemicals have the capacity to damage the human brain, and they conclude that chemical pollution may have harmed the brains of millions of children worldwide. The authors conclude further that the toxic effects of industrial chemicals on children have generally been overlooked. In North Amercia, the commission for environmental cooperation, and in European Union the DEVNERTOX projects had reached to the same conclusions. We analyse this review and discuss these rather pessimistic conclusions."
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  32. Strategies for the prevention of environmental neurotoxic illness. Landrigan PJ, Graham DG, Thomas RD, Environ Res 1993 Apr;61(1):157-63
    " Toxic chemicals in the environment can cause a wide range of neurological disease.... Environmental neurotoxicants have also been shown to produce a wide range of subclinical neurotoxic effects, including reduction in intelligence, impairment in reasoning ability, shortening of attention span, and alternation of behavior. The first step in the prevention of environmental neurotoxicity is to test chemicals for their toxic potential. More than 70,000 chemicals are currently in commerce. However, except for pharmaceuticals, fewer than 10% of these chemicals have been tested for neurotoxicity. ... Screening programs ... designed to detect excessive absorption of a neurotoxic agent or subclinical neurological dysfunction can be useful in identifying affected individuals before severe disability occurs."
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  33. Attention-Deficit/Hyperactivity Disorder: A Preventable Epidemic? Lanphear, BP. Archives of Pediatric & Adolescent Medicine, 166(12), 1182-4.
    "Some critics have argued that the concentrations of environmental contaminants routinely found in pregnant women and children are too low to be biologically active. Yet, therapeutic levels of methylphenidate, the most commonly prescribed drug used to modify ADHD symptoms in children,3 are comparable to the concentrations in which the toxic effects of some environmental contaminants have been observed."
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  34. Workshop on perinatal exposure to dioxin-like compounds. I. Summary. Lindstrom G, Hooper K, Petreas M, Stephens R, Gilman, Environ Health Perspect 1995 Mar;103 Suppl 2:135-42
    "An international workshop reviewed 20 ongoing or recently completed studies of the effects of perinatal exposures to dioxins, dibenzofurans, and PCBs on the reproductive, endocrine, neurodevelopmental, and immune systems. Many of the observed effects are consistent with these compounds acting as "environmental hormones" or endocrine disrupters..."
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  35. Neonatal effects of toluene on the locomotor behavioral development of the rat. Lorenzana-Jimenez M, Salas M, Neurobehav Toxicol Teratol 1983 May-Jun;5(3):295-9
    "Rats were exposed to toluene twice a day for a period of 15 minutes on Days 2 through 32 of postnatal life... Maturation of swimming behavior and physical development were delayed ... escape from water showed prolonged mean latencies ... locomotor activity was increased during the 60 minutes following toluene exposure, compared with non-exposed littermate controls..." Exposure of rats to neurotoxic substances commonly results in hyperactivity, as though the "brakes" are the neurons first suffering damage. Toluene is a solvent made from petroleum or coal tar. Its chemical formula is C6H5CH3

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  36. Organic Diets Significantly Lower Children's Dietary Exposure to Organophosphorus Pesticides. Lu C, Toepel K, Irish R, Fenske RA, Barr DB, Bravo R., Environ Health Perspect. 2006 Feb;114(2):260-3.
    ". . . We substituted most of children's conventional diets with organic food items for 5 consecutive days and collected two spot daily urine samples, first-morning and before-bedtime voids, throughout the 15-day study period. We found that the median urinary concentrations of the specific metabolites for malathion and chlorpyrifos decreased to the nondetect levels immediately after the introduction of organic diets and remained nondetectable until the conventional diets were reintroduced. . . In conclusion, we were able to demonstrate that an organic diet provides a dramatic and immediate protective effect against exposures to organophosphorus pesticides that are commonly used in agricultural production. We also concluded that these children were most likely exposed to these organophosphorus pesticides exclusively through their diet. To our knowledge, this is the first study to employ a longitudinal design with a dietary intervention to assess children's exposure to pesticides. It provides new and persuasive evidence of the effectiveness of this intervention."
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  37. Blood lead levels and behaviour of 400 preschool children. McBride WG, Black BP, English BJ, Med J Aust 1982 Jul 10;2(1):26-9
    " A study of 400 Sydney children of preschool age has found a range of blood lead levels ...2 micrograms/100 mL to 29 micrograms/100 mL... Within the range of blood lead levels, no relationship appeared between blood lead levels and performance in verbal intelligence test, three of the tests of motor ability, and a parent rating. In one of the tests of fine motor coordination, there was a tendency for the children with lower lead levels to perform better than those with moderate blood lead levels. ... Further studies of a prospective nature covering the period of maximum vulnerability (0 to three years) are essential before any conclusion can be drawn about the effects of subclinical blood levels of lead."
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  38. Lead poisoning associated with imported candy and powdered food coloring--California and Michigan. MMWR Morb Mortal Wkly Rep. 1998 Dec 11;47(48):1041-3.
    " Although the most common source of pediatric lead poisoning is dust within the home that contains deteriorated lead-based paint from walls and windowsills, other less common sources (1-3) can result in excess exposure among children . . . This report describes two cases of pediatric lead poisoning associated with eating imported candy and food stuffs and underscores the importance of thorough history-taking to identify unusual sources of lead exposure. "

    We wonder why this does not underscore the importance of getting the lead out of artificial food colorings?

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  39. Behavioral and neurochemical alterations in the offspring of rats after maternal or paternal inhalation exposure to the industrial solvent 2-methoxyethanol. Nelson BK, Brightwell WS, Burg JR, Massari VJ, Pharmacol Biochem Behav 1984 Feb;20(2):269-79
    "The industrial solvent 2-methoxyethanol (2ME) has antifertility effects in male rats at 300 ppm and is teratogenic in rats and rabbits at 50 ppm. The present research investigated if exposure of paternal or maternal animals to 25 ppm 2ME, the current U.S. permissible occupational exposure limit, would produce detectable effects in the offspring. ... changes were numerous in the brainstem and cerebrum but were fewer in the cerebellum and midbrain. Thus it appears that both paternal and maternal inhalation of 25 ppm 2ME produces some effect which is reflected in neurochemical deviations in the offspring."
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  40. The Examination of the Link Between Pesticides in Food and Learning Disorders in Children. Raby SE, Master's Thesis, Dominican College.
    "The relationship between pesticides in food and the occurrence of attention deficit disorder (ADD) and attention deficit hyperactivity disorder (ADHD) in school age children is considered. . . Medical research is cited that links damage to neurotransmitters in the brain's frontal lobes and ADD/ADHD. Evidence showing that pesticides can damage brain cells is also presented. Problems with the detection of pesticide residues in foods are acknowledged. The treatment of ADD/ADHD has commonly been to medicate the child with stimulant drugs that affect the body's neurotransmitter chemicals, as well as tricyclic antidepressants and tranquilizers. Dietary treatment, behavior modification, and stress reduction therapies may be additional treatment options. . ."
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  41. Bisphenol A in dental sealants and its estrogen like effect.
    Rathee M, Malik P, Singh J. Indian J Endocrinol Metab. 2012 May;16(3):339-42. doi: 10.4103/2230-8210.95660.
    " Bisphenol A or BPA-based epoxy resins are widely used in the manufacture of commercial products, including dental resins, polycarbonate plastics, and the inner coating of food cans. BPA is a precursor to the resin monomer Bis-GMA. During the manufacturing process of Bis-GMA dental sealants, Bisphenol A (BPA) might be present as an impurity or as a degradation product of Bis-DMA through esterases present in saliva. Leaching of these monomers from resins can occur during the initial setting period and in conjunction with fluid sorption and desorption over time and this chemical leach from dental sealants may be bioactive. Researchers found an estrogenic effect with BPA, Bis-DMA, and Bis-GMA because BPA lacks structural specificity as a natural ligand to the estrogen receptor. It generated considerable concern regarding the safety of dental resin materials. This review focuses on the BPA in dental sealants and its estrogen-like effect. "
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  42. Exposure to Hexachlorobenzene during Pregnancy and Children's Social Behavior at 4 Years of Age. Ribas-Fitó N, Torrent M, Carrizo D, Júlvez J, Grimalt JO, Sunyer J., Environmental Health Perspectives, 2007 Mar;115(3):447-50. Epub 2006 Nov 6.
    "Hexachlorobenzene (HCB) is an organochlorine chemical that has been used in agriculture and industrial processes... Our goal was to study the association of prenatal exposure to HCB with the social behavior of preschool children... RESULTS: Children with concentrations of HCB > 1.5 ng/mL at birth had a statistically significant increased risk of having poor Social Competence ... and ADHD ... scores. . . ."
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  43. Clinical characteristics of chemical sensitivity: an illustrative case history of asthma and MCS. Ross GH, Environ Health Perspect 1997 Mar;105 Suppl 2:437-41
    "A case history of the induction of asthma and chemical sensitivity in a 42-year-old registered nurse illustrates several of the characteristic features of multiple chemical sensitivity (MCS). This patient's problems started shortly after moving into a new home under construction, with associated chemical exposures... Patients often describe a spreading phenomenon of increasing intolerance to commonly encountered chemicals at concentrations well tolerated by other people. Symptoms ... are more likely to occur in patients or families with preexisting histories of migraine or with classical allergies. ... Myalgia and joint pains and food intolerance are common features as well. Contamination with xenobiotic chemicals is frequently found in these patients when they are tested. Reactive airways dysfunction syndrome is a recently identified condition that exhibits features of both asthma and chemical sensitivity. MCS patients frequently have patterns of neurotoxic brain metabolism that can be confirmed on single photo emission computed tomography imaging."
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  44. Prenatal exposure to methylmercury alters locomotor activity of male but not female rats. Rossi AD et al., Exp Brain Res 1997 Dec;117(3):428-36
    "... A significant decrease in spontaneous motility and rearing was observed only in the MeHg-treated male rats. ... Taken together, these findings show that during development a very low dosage of MeHg [methyl mercury] exerts neurotoxic effects detectable in adulthood, and that susceptibility is gender-dependent."
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  45. Development of locomotor activity of rat pups exposed to heavy metals. Ruppert PH, Dean KF, Reiter LW, Toxicol Appl Pharmacol 1985 Mar 30;78(1):69-77
    "Cadmium (Cd), triethyltin (TET), and trimethyltin (TMT) are heavy metals which are neurotoxic to developing animals. ... A single exposure to Cd, TET, and TMT produced hyperactivity by the end of the preweaning period but these metals differed in the day of peak activity, the onset of hyperactivity, and the development of habituation."
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  46. Prenatal organochlorine exposure and behaviors associated with attention deficit hyperactivity disorder in school-aged children. Sagiv SK, Thurston SW, Bellinger DC, Tolbert PE, Altshul LM, Korrick SA. American Journal of Epidemiology, 2010 Mar 1;171(5):593-601. Epub 2010 Jan 27.
    "Organochlorines are environmentally persistent contaminants that readily cross the placenta, posing a potential risk to the developing fetus. Evidence for neurodevelopmental effects at low levels of these compounds is growing, though few studies have focused on behavioral outcomes. The authors investigated the association between prenatal polychlorinated biphenyl (PCB) and p,p'-dichlorodiphenyl dichloroethylene (p,p'-DDE) levels and behaviors associated with attention deficit hyperactivity disorder (ADHD), measured with the Conners' Rating Scale for Teachers (CRS-T), in a cohort of 607 children aged 7-11 years (median age, 8.2 years) born in 1993-1998 to mothers residing near a PCB-contaminated harbor in New Bedford, Massachusetts. . . the authors found higher risk of atypical behavior on the Conners' ADHD Index for the highest quartile of the sum of 4 PCB congeners versus the lowest quartile . . . These results support an association between low-level prenatal organochlorine exposure and ADHD-like behaviors in childhood."
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  47. Toxic threats to neurologic development of children. Schettler T., Environmental Health Perspectives, 2001 Dec;109 Suppl 6:813-6.
    "Learning disabilities, attention deficit hyperactivity disorder, developmental delays, and emotional and behavioral problems are among childhood disabilities of increasing concern. Interacting genetic, environmental, and social factors are important determinants of childhood brain development and function. . . . Historically, understanding the effects of these toxicants on the developing brain has emerged slowly while generations of children are exposed to unsafe levels. Unfortunately, with few exceptions, neurodevelopmental toxicity data are missing for most industrial chemicals in widespread use, even when populationwide exposures are documented. The personal, family, and communitywide costs of developmental disabilities are profound. In addition to the need for more research, a preventive public health response requires mitigation of exposures to potential neurodevelopmental toxicants when available evidence establishes the plausibility of harm, despite residual toxicologic uncertainties."
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  48. Chronic lead exposure induces alterations on local circuit neurons. Selvin-Testa A, Microsc Electron Biol Celular 1991 Jun;15(1):25-39
    "... Chronic lead [in a low dose] was administered to rat pups... Electron microscopy studies were made at 30, 45, 60, 75 and 90 days of age. ... These results suggested that the functional activity of LCN could be modified by the observed changes. Such ultrastructural modifications could be a morphological substrate for the subtle neuropsychological deficits of rats chronically exposed to relatively low concentration of lead."
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  49. An updated review of environmental estrogen and androgen mimics and antagonists. Sonnenschein C, Soto AM, J Steroid Biochem Mol Biol 1998 Apr;65(1-6):143-50
    "For the last 40 y, substantial evidence has surfaced on the hormone-like effects of environmental chemicals such as pesticides and industrial chemicals in wildlife and humans. The endocrine and reproductive effects of these chemicals are believed to be due to their ability to: (1) mimic the effect of endogenous hormones, (2) antagonize the effect of endogenous hormones, (3) disrupt the synthesis and metabolism of endogenous hormones, and (4) disrupt the synthesis and metabolism of hormone receptors. ... Aviation crop dusters handling DDT were found to have reduced sperm counts,... Man-made compounds used in the manufacture of plastics were accidentally found to be estrogenic because they fouled experiments conducted in laboratories studying natural estrogens. For example, polystyrene tubes released nonylphenol, and polycarbonate flasks released bisphenol-A. ... Bisphenol-A was found to contaminate the contents of canned foods; these tin cans are lined with lacquers such as polycarbonate. Bisphenol-A is also used in dental sealants and composites. We found that this estrogen leaches from the treated teeth into saliva; ... These compounds act cumulatively. ... It has been hypothesized that endocrine disruptors may play a role in the decrease in the quantity and quality of human semen during the last 50 y, as well as in the increased incidence of testicular cancer and cryptorchidism in males and breast cancer incidence in both females and males in the industrialized world. ..."
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  50. Effects of long-term oral administration of DDT on nonhuman primates. Takayama S, Sieber SM, Dalgard DW, Thorgeirsson UP, Adamson RH, J Cancer Res Clin Oncol 1999;125(3-4):219-25
    " . . . a decision was made in 1969 to evaluate the long-term effects of DDT on 24 cynomolgus and rhesus monkeys. . . Benign tumors detected in the DDT group included three cases of leiomyoma, two of which were uterine and one, esophageal. No tumor was detected in the control group of 17 monkeys. Fatty changes in the liver were observed in 52.9% of the DDT group and 29.4% of the control group. More specific signs of hepatotoxicity were documented microscopically in seven DDT monkeys. Severe tremors and histological evidence of CNS and spinal cord abnormalities were observed in six DDT monkeys. The present findings show clear evidence of hepatic and CNS toxicity following long-term DDT administration to cynomolgus and rhesus monkeys. However, the two cases involving malignant tumors of different types are inconclusive with respect to a carcinogenic effect of DDT in nonhuman primates. "
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  51. Postnatal exposure to benzene alters the neurobehavioral functioning of rats when tested during adulthood. Tilson HA, Squibb RE, Meyer OA, Sparber SB, Neurobehav Toxicol 1980 Summer;2(2):101-6
    "... The spontaneous motor activity of benzene exposed rats (males and females) was found to be elevated when tested at 100-130 days of age. ... These data indicate that postnatal exposure to benzene can produce significant alterations in the motor activity of rats when tested during adulthood ... Changes in the sensitivity of benzene exposed animals to d-amphetamine suggest long-term alterations in catecholaminergic function."
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  52. Pneuropsychological disorders after occupational exposure to mercury vapors in El Bagre (Antioquia, Colombia) Tirado V, Garcia MA, Moreno J, Galeano LM, Lopera F, Franco A., Rev Neurol. 2000 Oct 16-31;31(8):741-2
    " ... In the gold-producing regions the population is exposed to high levels of mercury used in the processes of extraction and purification. ... the effect of long-term exposure on cognitive function has not been studied. ... In the study group alterations were seen and classified as: intellectual damage (mainly alteration of executive function and constructional praxis); emotional changes (symptoms of depression and anxiety) and neurological changes (amnesia, insomnia and tremor of the tongue). No changes were found in the control group. CONCLUSION: Exposure to mercury causes specific neuropsychological and behavior disorders in the absence of clinically detectable physical or physiological damage. "
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  53. Selenium deficiency and brain functions: the significance for methylmercury toxicity Watanabe C., Nippon Eiseigaku Zasshi 2001 Jan;55(4):581-9
    " ... Since iodothyronine deiodinases (DIs), which regulate the tissue levels of thyroid hormone, are (likely to be) selenoproteins, Se might have specific roles for developing brain. ... When the animals were depleted of Se after weaning, when the role of thyroid hormone on brain development is minimal, neurochemical and neurophysiological alterations were found in the dopaminergic system. These postnatally-depleted rodents also showed abnormal open-field behavior, which was distinct from that observed with perinatally-depleted animals. ... Experimental findings showed that Se-deficient rodents are more susceptible to the prenatal toxicity of MeHg. It is noteworthy that MeHg specifically altered the metabolism of Se in fetal/neonatal brain. ... "
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  54. Behavior as an early indicator of pesticide toxicity. Weiss B., Toxicol Ind Health. 1988 Sep;4(3):351-60.
    " Adverse behavioral effects are now a recognized outcome of exposure to many industrial and environmental chemicals. Pesticides occupy a special role, however, because so many of them, particularly insecticides, are designed specifically to act on neural tissue. The evaluation of behavioral toxicity is a new kind of challenge to pesticide toxicology because of the enormous structural and chemical heterogeneity of the nervous system and the even greater complexity of behavior. . . "
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  55. A risk assessment perspective on the neurobehavioral toxicity of endocrine disruptors. Weiss B. Toxicol Ind Health. 1998 Jan-Apr;14(1-2):341-59.
    " ... The primary distinction between cancer and endocrine disruptors and neurotoxicants is the plethora of possible endpoints by which toxicity can be expressed. Cancer is a unitary index. Adverse consequences flowing from exposure to endocrine disruptors can take an almost infinite variety of forms, including neurobehavioral outcomes. In their most troubling manifestations, these emerge as disorders of early development. They can range from deviant patterns of male copulatory behavior to impaired cognitive function. Each of these indices, in turn, exhibits multiple dimensions. Moreover, some aftermaths, as with cancer, might emerge only after long latencies. Different stages of the life cycle following developmental exposure will manifest different outcomes as a consequence. Some adverse effects may arise for the first time in advanced age because it is a period of declining compensatory margins. These multiple facets of neurobehavioral toxicity, and, by extension, their coupling to endocrine disruptors, imply a risk assessment process that corresponds, in many ways, to the global views adopted by ecotoxicologists. "
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  56. Effects of toluene inhalation on locomotor activity and brain catecholamine levels in rats. Yamawaki S, Sarai K, Yakubutsu Seishin Kodo 1982 Jul;2(1):57-9
    "...The inhaling of toluene vapor (0.7% in air, for 15 min) induced the increase in spontaneous locomotor activity. This locomotor accelerating effect lasted about 60 min after the end of toluene exposure. ... These results suggest that toluene may raise dopaminergic neuron activity."

    Toluene is a solvent made from petroleum or coal tar. Its chemical formula is C6H5CH3

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