Triorthocresyl Phosphate Poisoning

Inoue, Naoki; Fujishiro, Kazuya; Mori, Koji; Matsuoka, Masato

doi:10.7888/juoeh.10.433

Cited by 24 publications

(18 citation statements)

References 2 publications

(2 reference statements)

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“…The late appearance of lowerextremity spasticity consistent with pyramidal tract involvement is the only established CNS disorder associated with OP intoxication. 5,39 The proposed COPIND remains a poorly characterized collection of symptoms and signs that has been attributed to chronic low-level exposure to OP compounds at levels insufficient to produce cholinergic symptoms. 1,2 Cognitive impairments have been reported in association with low-dose exposure to OP compounds.…”

Section: Discussionmentioning

confidence: 99%

The Effects of Occupational Exposure to Chlorpyrifos on the Neurologic Examination of Central Nervous System Function: A Prospective Cohort Study

Albers

Berent

Garabrant

et al. 2004

Journal of Occupational and Environmental Medicine

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Questions persist about adverse effects such as impaired cognition and attention, incoordination, spasticity, or parkinsonism from chronic, low-level exposures to organophosphate (OP) compounds. In a prospective cohort study, we evaluated chlorpyrifos-manufacturing workers and a referent group on 2 occasions, 1 year apart, to determine whether occupational exposure to chlorpyrifos produced clinically evident central nervous system (CNS) dysfunction. Chlorpyrifos subjects had significantly higher TCP excretion and lower average BuChE activity than referents in a range in which physiological effects on B-esterases exist. Few subjects had neurologic symptoms or signs, and there were no significant group differences in terms of signs at baseline or second examinations. Chronic chlorpyrifos exposure produced no clinical evidence of cortical, pyramidal tract, extrapyramidal, or other CNS dysfunction among chlorpyrifos subjects compared with referents, either at baseline or after 1 year of additional chlorpyrifos exposure.

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Section: Discussionmentioning

confidence: 99%

The Effects of Occupational Exposure to Chlorpyrifos on the Neurologic Examination of Central Nervous System Function: A Prospective Cohort Study

Albers

Berent

Garabrant

et al. 2004

Journal of Occupational and Environmental Medicine

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“…All three cases had severe neurologic abnormalities, but experienced extensive if not complete recovery. Inoue et al (1988) cited two additional cases in German chemical plants (1943,1946) but gave no details. Bidstrup and Bonnel (1954) …”

Section: Experience With the Use Of Tcp In The Industrial Environmentmentioning

confidence: 99%

“…The hazards of TCP exposure were first recognized from cases of human intoxication (Zinn, 1968;Inoue et al, 1988). However, most of the toxicology of the aryl phosphates comes from the study of experimental animals, particularly the mature hen and cat (Smith et al, 1930a;Abou-Donia et al, 1986).…”

mentioning

confidence: 99%

“…In the last century as many as 60,000 people may have suffered delayed neuropathy as a result of contamination of food or beverages by industrial products containing aryl phosphate esters, mainly TCP (Zinn, 1968;Inoue et al, 1988). Poisoning has resulted from ingestion of oils containing as little as 3% TCP (Inoue et al, 1988).…”

mentioning

confidence: 99%

“…Poisoning has resulted from ingestion of oils containing as little as 3% TCP (Inoue et al, 1988). The episodes have occurred worldwide and under a wide variety of circumstances, both intentional and accidental.…”

mentioning

confidence: 99%

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Evaluation of the hazards of industrial exposure to tricresyl phosphate:a review and interpretation of the literature

Craig¹

1999

Journal of Toxicology and Environmental Health, Part B

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Commercial tricresyl phosphate (TCP) is a heterogeneous mixture of isomers and aryl phosphate congeners, known for many years to induce delayed neurotoxicity (OPIDN) in humans and experimental animals. In the past the isomer tri-o-cresyl phosphate (TOCP) was thought to be the component primarily responsible for OPIDN. It is now clear that other constituents, particularly the mono-o-esters, are not only neurotoxic but also may be more potent than pure TOCP. As a generality, the toxicity potential of a particular brand of TCP is related to its content of o-phenolic residues, whereby the maximal potential is reached when o-phenolics are 33% of the mix. Historically, human TCP toxicity has resulted from inadvertent or intentional contamination of foodstuffs or beverages. TCP products with high ortho-residues synthesized by older manufacturing methods were involved in most of these cases, and were likely much more neurotoxic milligram for milligram than TOCP. Because of the great variability of TCP products, there are no conventional workplace exposure standards. Based upon data from the hen and cat, estimated human safe exposure rates for pure TOCP are estimated to be 2.5 mg/kg for a single dose, and 0.13 mg/kg/d for repetitive exposures. These levels may also be applied to TCP when o-methyl-phenyl, o-ethyl-phenyl, and o-xylenyl components are appropriately limited during manufacture such that the TCP product is less neurotoxic than TOCP. There have been relatively few reports of toxicity associated with the manufacture or use of TCP in commerce and industry. Low vapor pressures of the constituents preclude the presence of significant quantities of TCP vapor in the atmosphere. A lubricant or other formulation containing TCP may appear in the air as a mist. By these criteria the U.S. Petroleum Oil Mist exposure standard is protective when the formulation contains 4% or less of low ortho-TCP. Exposure calculations indicate that estimated safe levels are not likely to be exceeded in the well-regulated workplace. If it is of short duration, even a heavy fog of oil particulate may not exceed the 8-h-average inhalation exposure standard. Modern manufacturing practices tend to minimize the ortho content and thus the toxicity of TCP. Because individual TCP brands and synthesis methods vary, manufacturers should be consulted concerning the properties of their individual products.

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Tea polyphenols alleviate tri‐ortho‐cresyl phosphate‐induced autophagy of mouse ovarian granulosa cells

Yang

Shao

Huang

et al. 2019

Environmental Toxicology

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Tri‐ortho‐cresyl phosphate (TOCP), a widely used plasticizer in industry, can cause female reproductive damage. Tea polyphenols (TPs) have multiple health effects via inhibiting oxidative stress. However, the reproductive protection of TPs in TOCP‐induced female reproductive system damage is yet to be elucidated. In the study, TOCP inhibited cell viability and induced autophagy of mouse ovarian granulosa cells; while TPs could rescue the inhibition of viability and induction of autophagy. 3‐MA, an autophagy inhibitor, could also rescue the inhibition of cell viability. These results indicated that TPs played a protective role in TOCP‐induced autophagy. Furthermore, TPs could inhibit the induction of oxidative stress of the cells by TOCP, which implying that TPs might alleviate TOCP‐induced autophagy via inhibiting oxidative stress. Furthermore, TPs could rescue TOCP‐induced autophagy and oxidative stress in the mouse ovarian tissues. Taken together, these results indicated that TPs could protect TOCP‐induced ovarian damage via inhibiting oxidative stress.

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Triorthocresyl Phosphate Poisoning

Cited by 24 publications

References 2 publications

The Effects of Occupational Exposure to Chlorpyrifos on the Neurologic Examination of Central Nervous System Function: A Prospective Cohort Study

The Effects of Occupational Exposure to Chlorpyrifos on the Neurologic Examination of Central Nervous System Function: A Prospective Cohort Study

Evaluation of the hazards of industrial exposure to tricresyl phosphate:a review and interpretation of the literature

Tea polyphenols alleviate tri‐ortho‐cresyl phosphate‐induced autophagy of mouse ovarian granulosa cells

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