Formaldehyde 2% is not a useful means of detecting allergy to formaldehyde releasers- results of the ESSCA network, 2015-2018.

BACKGROUND: Studies suggest that patch testing with formaldehyde releasers (FRs) gives significant additional information to formaldehyde 1% aq. and should be considered for addition to the European baseline series (EBS). It is not known if this is also true for formaldehyde 2% aq. OBJECTIVES: To determine the frequency of sensitization to formaldehyde 2% aq. and co-reactivity with FRs. To establish whether there is justification for including FRs in the EBS. MATERIALS AND METHODS: A 4-year, multi-center retrospective analysis of patients with positive patch test reactions to formaldehyde 2% aq. and five FRs. RESULTS: A maximum of 15 067 patients were tested to formaldehyde 2% aq. and at least one FR. The percentage of isolated reactions to FR, without co-reactivity to, formaldehyde 2% aq. for each FR were: 46.8% for quarternium-15 1% pet.; 67.4% imidazolidinyl urea 2% pet.; 64% diazolidinyl urea 2% pet.; 83.3% 1,3-dimethylol-5, 5-dimethyl hydantoin (DMDM) hydantoin 2% pet. and 96.3% 2-bromo-2-nitropropane-1,3-diol 0.5% pet. This demonstrates that co-reactivity varies between FRs and formaldehyde, from being virtually non-existent in 2-bromo-2-nitropropane-1,3-diol 0.5% pet. (Cohen's kappa: 0, 95% confidence interval [CI] -0.02 to 0.02)], to only weak concordance for quaternium-15 [Cohen's kappa: 0.22, 95%CI 0.16 to 0.28)], where Cohen's kappa value of 1 would indicate full concordance. CONCLUSIONS: Formaldehyde 2% aq. is an inadequate screen for contact allergy to the formaldehyde releasers, which should be considered for inclusion in any series dependant on the frequency of reactions to and relevance of each individual allergen.

Formaldehyde-releasers in cosmetics: relationship to formaldehyde contact allergy. Part 2. Patch test relationship to formaldehyde contact allergy, experimental provocation tests, amount of formaldehyde released, and assessment of risk to consumers allergic to formaldehyde.

This is the second part of an article on formaldehyde-releasers in cosmetics. The patch test relationship between the releasers in cosmetics to formaldehyde contact allergy is reviewed and it is assessed whether products preserved with formaldehyde-releasers may contain enough free formaldehyde to pose a threat to individuals with contact allergy to formaldehyde. There is a clear relationship between positive patch test reactions to formaldehyde-releasers and formaldehyde contact allergy: 15% of all reactions to 2-bromo-2-nitropropane-1,3-diol and 40-60% of the reactions to the other releasers are caused by a reaction to the formaldehyde in the test material. There is only fragmented data on the amount of free formaldehyde in cosmetics preserved with formaldehyde donors. However, all releasers (with the exception of 2-bromo-2-nitropropane-1,3-diol, for which adequate data are lacking) can, in the right circumstances of concentration and product composition, release >200 p.p.m. formaldehyde, which may result in allergic contact dermatitis. Whether this is actually the case in any particular product cannot be determined from the ingredient labelling. Therefore, we recommend advising patients allergic to formaldehyde to avoid leave-on cosmetics preserved with quaternium-15, diazolidinyl urea, DMDM hydantoin, or imidazolidinyl urea, acknowledging that many would tolerate some products.

Occupational allergic contact dermatitis to nitromethane.

Nitromethane has wide industrial and commercial application as a polar solvent for adhesives and acrylics as well as explosive fuel. Allergic contact dermatitis to this chemical has not been described previously. The authors documented allergic contact hand dermatitis in 4 coworkers who similarly handled an adhesive solvent containing nitromethane. All 4 cases were confirmed by patch testing and resolved after allergen avoidance.

Peripheral neuropathy in workers exposed to nitromethane.

BACKGROUND: Two workers from a headlight subassembly plant developed severe peripheral neuropathy. These workers had extensive, but brief (1-2 months) dermal and inhalational exposure to nitromethane, a solvent. METHODS: Environmental sampling was performed for nitromethane and ethyl cyanoacrylate. Medical records, including electrodiagnostic studies, were reviewed. Literature on nitromethane, ethyl cyanoacrylate, and other exposures in the workplace was reviewed. RESULTS: Electromyography and nerve conduction studies performed on these patients were consistent with a severe, axonal neuropathy. No etiology was discovered despite an extensive medical evaluation. Environmental sampling revealed exposure to nitromethane at the threshold limit value. CONCLUSIONS: The history of acute onset of severe peripheral neuropathy temporally associated with exposure to nitromethane is suggestive of a toxic neuropathy. While it cannot be definitively concluded that these two workers developed peripheral neuropathy secondary to exposures at work, occupational exposure to nitromethane appears to be the most likely etiology.

Effect of complex polyphenols and tannins from red wine (WCPT) on chemically induced oxidative DNA damage in the rat.

BACKGROUND: Flavonoids are polyphenolic antioxidants occurring in vegetables and fruits as well as beverages such as tea and wine which have been thought to influence oxidative damage. AIM OF THE STUDY: We wanted to verify whether a complex mixture of wine tannins (wine complex polyphenols and tannins, WCPT) prevent chemically-induced oxidative DNA damage in vivo. METHODS: Oxidative DNA damage was evaluated by measuring the ratio of 8-hydroxy-2'-deoxyguanosine (80HdG)/ 2-deoxyguanosine (2dG) x 10(-6) in hydrolyzed DNA using HPLC coupled with electrochemical and UV detectors. RESULTS: We treated rats with WCPT (57 mg/kg p.o.) for 14 d, a dose 10-fold higher than what a moderate wine drinker would be exposed to. WCPT administration significantly reduced the ratio of 80HdG/2dG x 10(-6) in liver DNA obtained from rats treated with 2-nitropropane (2NP) relative to controls administered 2NP only (33. 3 +/- 2.5 vs. 44.9 +/- 3.2 x 10(-6) 2dG; micro +/- SE; p<0.05). On the contrary, pretreatment with WCPT for 10 d did not protect the colon mucosa from oxidative DNA damage induced by 1, 2-dimethylhydrazine (DMH). 2NP and DMH are hepatic and colon carcinogens, respectively, capable of inducing oxidative DNA damage. CONCLUSIONS: WCPT have protective action against some types of chemically-induced oxidative DNA damage in vivo.

Prolonged formation of methemoglobin following nitroethane ingestion.

BACKGROUND: Artificial nail removers containing nitroethane pose a serious risk of toxicity when ingested. CASE REPORTS: We report 3 cases of children under 3 years of age who developed prolonged methemoglobinemia following ingestions of small quantities of these nitroethane-containing products. Methylene blue therapy reduced the methemoglobin level in all 3 children; however, in 2 of these children methemoglobin levels increased again several hours later and required additional methylene blue. Accurate substance identification is essential for appropriate management of ingestions of fingernail products. The availability of nitroethane products for home use should be questioned.

Unusual occupational toxins.

Occupational and environmental medicine affords encounters with many unusual toxins, ranging from exotic metals to rocket fuels. Twelve of the most unusual industrial toxins are reviewed here and their clinical manifestations and treatments explored: acetonitrile, acrylonitrile, boron hydrides, dimethylaminopropionitrile, dimethylformamide, hydrazines, methyl isocyanate, 2-nitropropane, phosphine, Stalinon, tellurium, and vanadium.

Relationship of hepatocarcinogenicity and hepatocellular proliferation induced by mutagenic noncarcinogens vs carcinogens. II. 1- vs 2-nitropropane.

2-Nitropropane (2-NP) is mutagenic in a number of short-term mutagenicity assays in vitro and in vivo, and is a potent hepatocarcinogen in rats. A structural isomer, 1-nitropropane (1-NP), is mutagenic in V79 cells and can induce unscheduled DNA synthesis in rat hepatocytes, yet did not induce tumors in rats following chronic exposure. We examined the correlation of cell proliferation and hepatocarcinogenesis induced by this mutagenic noncarcinogen-carcinogen pair in a rat liver proliferation model. Rats were exposed to gavage doses of 0.5, 1, or 2 mmol/kg of 1-NP or 2-NP daily for 10 days; the highest two dose groups were similar to the doses used in the carcinogenesis bioassay. Cell proliferation was quantitated by incorporation of bromodeoxyuridine, detected immunohistochemically, into newly synthesized DNA. Animals exposed to the vehicle exhibited a labeling index (LI) of approximately 1.9% and animals exposed to CCL4 had a LI of approximately 30%. Rats exposed to the hepatocarcinogen 2-NP exhibited a dose-related increase in LI to 6.3 and 11% at the 1 and 2 mmol/kg doses, respectively, and no increase above control at the 0.5 mmol/kg exposure level. Animals exposed to the noncarcinogenic isomer 1-NP showed no statistically significant increase in LI above controls at any dose level tested. Serum chemistries were consistent with mild to moderate decreases in hepatocellular function, cholestasis, and necrosis following 2-NP exposure, but only minimal effects were observed, probably due to slight dehydration resulting from 1-NP exposure. These data indicate a positive association between increased cell proliferation and hepatocarcinogenesis induced by these two nitropropane isomers.

Health examination and air monitoring evaluation for workers exposed to 2-nitropropane.

Comprehensive employee health examinations along with work-place area and personal monitoring were conducted to evaluate potential exposure to 2-nitropropane. The employee cross section included in the study consisted of nearly all workers at the plant. The entire workforce was represented, including those who did not have contact with 2-nitropropane. No adverse health effects were found which could be connected with work experience. Body systems evaluated included: lungs, liver, kidney, blood, skin and cardiovascular. Work area levels at specific locations sometimes exceeded 25 ppm, but personal time-weighted average levels generally were below 25 ppm.

Motor dysfunction following chronic exposure to a fluoroalkane solvent mixture containing nitromethane.

We report the occurrence of a partially reversible Parkinson-like extrapyramidal syndrome in a woman chronically exposed to vapours from an industrial solvent mixture based on trichlorotrifluoroethane and nitromethane. The fluoroalkane group of compounds has not been previously reported to produce such effects in man, but mixtures containing nitromethane may not be innocent. Under certain industrial conditions the conversion of nitromethane to methylisocyanide may result in toxicity particularly in the basal ganglia and cerebellum following chronic low level exposure.