Foliar phosphite application has minor phytotoxic impacts across a diverse range of conifers and woody angiosperms.

Phytophthora plant pathogens cause tremendous damage in planted and natural systems worldwide. Phosphite is one of the only effective chemicals to control broad-scale Phytophthora disease. Little work has been done on the phytotoxic effects of phosphite application on plant communities especially in combination with plant physiological impacts. Here, we tested the phytotoxic impact of phosphite applied as foliar spray at 0, 12, 24 and 48 kg a.i. ha(-1) . Eighteen-month-old saplings of 13 conifer and angiosperm species native to New Zealand, and two exotic coniferous species were treated and the development of necrotic tissue and chlorophyll-a-fluorescence parameters (optimal quantum yield, Fv /Fm ; effective quantum yield of photosystem II, ΦPSII ) were assessed. In addition, stomatal conductance (gs ) was measured on a subset of six species. Significant necrosis assessed by digital image analysis occurred in only three species: in the lauraceous canopy tree Beilschmiedia tawa (8-14%) and the understory shrub Dodonaea viscosa (5-7%) across phosphite concentrations and solely at the highest concentration in the myrtaceous pioneer shrub Leptospermum scoparium (66%). In non-necrotic tissue, Fv /Fm , ΦPSII and gs remained unaffected by the phosphite treatment. Overall, our findings suggest minor phytotoxic effects resulting from foliar phosphite application across diverse taxa and regardless of concentration. This study supports the large-scale use of phosphite as a management tool to control plant diseases caused by Phytophthora pathogens in plantations and natural ecosystems. Long-term studies are required to ascertain potential ecological impacts of repeated phosphite applications.

Triphenyl phosphite, a new allergen in polyvinylchloride gloves.

BACKGROUND: Contact allergy to polyvinylchloride (PVC) gloves has been reported relatively seldom. In spring 2011, 5 of our patients had patch test reactions to PVC gloves. We obtained a collection of PVC raw materials from industrial producers and suppliers of chemical compounds to be patch tested on patients with suspected PVC glove contact allergy. OBJECTIVES: To report the first results of these new test substances. METHODS: The patients were patch tested with the newly obtained test substances, plastics and glues series, and isocyanates and isocyanate prepolymers. We analysed nine PVC glove samples for triphenyl phosphate and its derivatives. RESULTS: Two patients reacted to a technical PVC antioxidant and one of its components, triphenyl phosphite (TPP). Contact allergy to TPP was very strong in 1 patient, and was the main cause of her hand dermatitis, whereas the other patient also had other contact allergies explaining her symptoms. Three patients reacted to their PVC gloves, but the specific allergen was not identified. Six PVC glove samples contained TPP at concentrations of 0.004-0.099%. TPP transforms into triphenyl phosphate during storage. CONCLUSIONS: TPP represents a new allergen in PVC gloves. It was detected in several PVC gloves in fairly high concentrations.

A quantitative assessment of TPP-induced delayed neuropathy in the retina and lateral geniculate nucleus of the European ferret (Mustela putorius furo).

Triphenyl phosphite (TPP) has been examined extensively in our lab to assess its degenerative effects on the visual pathway of the European ferret. Tanaka et al. [Fundam. Appl. ToxicoL 22 (1994) 577; J. Toxicol. Environ. Health 58 (1999) 215] reported an age-related pattern of fiber and cell body degeneration progressing from retinal axons and lateral geniculate nucleus (LGN) neurons to the visual cortex. These studies, however, did not address whether TPP exposure results in retinal ganglion cell (RGC) degeneration, nor did they quantify the degenerative effects in the LGN. The purpose of this study was to quantify the effects of TPP on RGCs and LGN neurons. We administered single subcutaneous injections of TPP (1184 mg/kg) to 13 ferrets for histological analysis. The retinae were examined as whole-mounts and the brains sectioned parasagittally (50 microm). RGC countsfrom matched areas of nasal retina showed significantly fewer (21%) neurons in the TPP-treated ferrets (Sd = 282 +/- 52S.D.; 7d = 284 +/- 12S.D.) compared with control (359 +/- 42S.D.). No significant difference in cell number was found in temporal retina, even though this region contained, on average, 13% fewer ganglion cells in TPP-treated ferrets (Sd = 3344 +/- 44S.D.; 7d = 357 +/- 39S.D. versus control = 394 +/- 72S.D.). The mean soma sizes and RGC cell size distributions for nasal and temporal retinae were not significantly different for any group. LGN neurons were significantly smaller (28%) than control in the TPP-treated ferrets (Sd = 155 microm2 +/- 23S.D.; 7d = 152 microm2 +/- 28S.D. versus control = 214 microm2 +/- 9S.D.). Cell size distributions for LGN neurons were shifted toward smaller cell sizes in both TPP-treated groups compared to control.

[A review of studies of the delayed neurotoxicity induced by organophosphorus esters].

Organophosphorus esters have been used in the plastics industry as antioxidants and plasticizers, in agriculture as insecticides, and in the military as nerve agents. Some of these compounds have organophosphorus ester-induced delayed neurotoxicity (OPIDN) different from the acute toxicity caused by the acetylcholine esterase inhibiting activity. this review describes recent progress in studies on OPIDN and, discusses the future direction of studies. OPIDN is characterized by a more than 7 day incubation period, lower limb paralysis accompanied by axonal degeneration, and age- and species-specificity. Younger animals and rodents are not very sensitive to OPIDN. As well as fast recovery of inhibited neurotoxic esterase or neuropathy target esterase (NTE) in the sciatic nerve, detoxicating mechanisms including carboxylesterases are contributing to age- and species-specificity for OPIDN. Although, anterograde axonal transport does not seem to be affected by OPIDN, slow down of retrograde axonal transport was observed. Inhibition of NTE, and aging of inhibited NTE has been thought to be responsible for OPIDN, but there are some arguments against the role of NTE in OPIDN. Phosphorylation of cytoskeletal proteins by kinases such as calcium dependent-calmodulin kinase II and/or high affinity neurotoxic compound binding site(s) are possible candidates for the initiation of OPIDN. Triphenyl phophite (TPP), a compound commonly used in the plastics industry, has delayed neurotoxicity that is somewhat different from OPIDN. The onset of TPP-induced neuropathy is earlier than that of OPIDN, and rodents are sensitive to TPP. In addition to the axonal damage, cell damage is observed in TPP-induced neuropathy. Mitochondrial energy metabolism-related enzymes could be the target of this neuropathy. Future studies should be focused on the relation of OPIDN to the phosphorylation of cytoskeletal proteins and high affinity binding site(s), and on the development of rodent models. These studies would answer the questions related to OPIDN, and further contribute toward elucidating the pathogenesis of degenerative neuronal diseases.