A comparative study of formaldehyde detection using chromotropic acid, acetylacetone and HPLC in cosmetics and household cleaning products

Chromotropic acid and acetylacetone methods for qualitative determination of formaldehyde were tested in parallel on 48 commercial samples, with high-performance liquid chromotography (HPLC) implemented for quantitative measure. In addition, interference with the detection of formaldehyde was investigated by analyzing 12 other aldehydes and ketones, 7 essential oils and 3 polysorbates. Throughout this comparative study, the disadvantages of the chromotropic acid method, of which 2 variants were used, were delineated and we found that the acetylacetone test proved to be a more efficient screening method for formaldehyde detection in a clinical laboratory.     

Fluorescence spectroscopy monitoring of the conformational restraint of formaldehyde- and glutaraldehyde- treated infectious bursal disease virus proteins

Interaction of native proteinaceous antigens during the recognition and the effector phases of an immune response leads to antigenic conformational modifications which may elicit additional specific immune response. Protein cross-linking and conformation restraining formaldehyde and glutaraldehyde have been extensively used in vaccine preparation, but the relative efficiencies of conformational restraint at concentrations similar to those used in vaccine preparation have not been investigated. We addressed this issue by comparing the extent of conformational restraint of virus proteins in formaldehyde- and glutaraldehyde-treated virus preparations by monitoring the fluorescence intensities (I₃₂₀) of infectious bursal disease virus preparations (IBDV) and those of untreated virus during thermal denaturation. Formaldehyde was found to cause no detectable conformational restraint at 0.01% and only very weak restraint at 1%, while glutaraldehyde caused very strong conformational restraint at 0.01%. It is proposed how conformational restraint of proteinaceous antigens may alter ensuing immunity.     

Anaphylaxis after dental treatment with a formaldehyde-containing tooth-filling material

A 67-year-old patient developed systemic reactions after application of a formaldehyde-containing tooth filling. She had a clearly positive RAST result for formaldehyde, whereas skin prick testing and patch tests were negative. Sensitization to formaldehyde appears to have occurred 1 year previously. Induction of formaldehyde allergy may represent a major complication during dental treatment, and assessment of specific IgE should he considered in patients at risk.     

Three Approaches to the Analysis of Trace Formaldehyde in Bulk and Dosage Form Pharmaceuticals

Trace-level determinations for the presence of formaldehyde in both bulk and dosage form pharmaceuticals were developed using three innovative strategies. One system adapted the chromotropic acid spot test for formaldehyde. This was accomplished spectrophotometrically over a linear detection range against authentic control samples. The other two chromatographic approaches necessitated rapid derivatization. One derivative was its corresponding oxime, formaldoxime, which was resolved on a gas chromatographic porous polymer column and sensed by a nitrogen-specific detector. The other derivative, sodium formate, was detected and quantified on an ion chromatograph using an anion-exchange column and a conductivity detector. The chromotropic acid technique was sensitive but not specific for formaldehyde. The chromatographic techniques required a high degree of water solubility. All were subject to interferences that could preclude their use for a particular application. None of the tested samples, which included a penicillin analogue, a pharmaceutical dosage form additive, a vitamin, and biological proteins, showed the presence of formaldehyde at trace levels.     

Inhibition of the acute ocular responses to nitrogen mustard by colchicine

Colchicine, a naturally occurring alkaloid, inhibits both fast and slow axoplasmic transport by prevention of microtubule assembly. We have examined the influence of colchicine on the neurogenically mediated acute inflammatory responses to topically administered nitrogen mustard and formaldehyde on the albino rabbit eye. Topical administration of colchicine (10, 20 or 40 micrograms) once per day for 15 days inhibited the ocular hypertensive response, the leakage of protein into the anterior chamber, and the pupillary constriction observed following topical administration of nitrogen mustard. Colchicine pretreatment also inhibited the ocular hypertensive response to topically administered formaldehyde. Pretreatment of the eye with colchicine (20 micrograms day-1) for a period of 5 days proved to be ineffective in suppressing the ocular hypertensive effect of nitrogen mustard, while more prolonged pretreatment (10 or 15 days) significantly abrogated the characteristic injury responses. Topical administration of colchicine (20 and 40 micrograms) caused dilation of conjunctival and limbal vessels, but these vascular responses subsided as treatment continued. These preliminary experiments suggest that the inhibition of the ocular responses to nitrogen mustard by chronic colchicine pretreatment might be the result of modification of synthesis or release of sensory mediator(s).     

Studies on reaction of formaldehyde with naturally occurring thiol compounds and ascorbic acid

To gain insight into possible cellular protective mechanisms against the insult of formaldehyde, we have investigated this molecule's reactivity with both naturally occurring thiol compounds including glutathione and L-ascorbic acid. By UV measurements, formaldehyde was found to rapidly react with glutathione forming an S-hydroxymethyl covalent adduct. The adduct which was confirmed by NMR is transiently stable. Formaldehyde is also significantly reactive with L-ascorbic acid in a reaction which was observed to be dissimilar to its reaction with dimedone. The reaction of formaldehyde with glutathione was reduced by 40% in the presence of an excess amount of L-ascorbic acid, due to the trapping of formaldehyde by L-ascorbic acid. The data suggest that L-ascorbic acid may have a possiblein vivo role in the metabolism of formaldehyde, thereby protecting cellular glutathione from possible depletion.     

Antibodies and immune profiles of individuals occupationally exposed to formaldehyde: Six case reports

Six patients with multiple subjective health complaints, which have been correlated with chronic exposure to formaldehyde during the course of their education and occupations, were tested for the existence of antibodies (IgE, IgM, and IgG) to formaldehyde (F) conjugated to human serum albumin (F-HSA). In addition, the percentage and absolute numbers of peripheral lymphocyte subpopulations as determined by surface markers were investigated. Antibody titers to F-HSA were present as follows: IgE (2 patients), IgM (3 of 4 tested patients), and IgG (5 patients). Analysis of lymphocyte subpopulations showed T-helper/suppressor (H/S) ratios ranging from 0.8 to 3.3. All 6 patients had elevated Tal cells (antigen memory cells), whereas interleuken 2 receptor positive cells were within expected values. Following formaldehyde exposure, 5 of the patients complained of an initial flulike illness from which they have not completely recovered. The sixth individual had a history of recurrent respiratory infections and surgical removal of hyperplastic ethmoid sinus tissue. The common occurrence of anti-F-HSA antibodies, flulike illness, and Tal cells are interpreted as suggestive of a chronic antigenic stimulation of the immune system in these 6 patients. Further immunological work-up of additional subjects and immune parameters with similar history of formaldehyde exposure and subjective health complaints is warranted.     

Formaldehyde exposure and lower respiratory infections in infants: findings from the PARIS cohort study

Background: Certain chemical pollutants can exacerbate lower respiratory tract infections (LRIs), a common childhood ailment. Although formaldehyde (FA) is one of the most common air pollutants found in indoor environments, its impact on infant health is uncertain.Objective: Our aim was to determine the impact of FA exposure on the LRI incidence during the first year of life of infants from the Pollution and Asthma Risk: an Infant Study (PARIS) birth cohort.Methods: FA was measured in a random sample of 196 infants’ dwellings, and exposure to this pollutant was estimated for 2,940 infants using predictive models based on measurements and data about potential determinants of FA levels. Health data were collected from parents by regular self-administered questionnaires. We used multivariate logistic regressions to estimate associations between FA exposure and the occurrence of LRI and wheezy LRI (wLRI), adjusting for potential confounders/risk factors.Results: During the first year of life, 45.8% of infants had at least one LRI, and LRI occurred simultaneously with wheezing in 48.7% of cases. The FA predictive models correctly classified 70% of dwellings as having high or low exposure, and we estimated that 43.3% of infants were exposed throughout the first year to levels of FA > 19.5 µg/m³. FA exposure was significantly associated with LRI and wLRI before and after adjustment for known LRI risk factors/confounders. For an interquartile increase in FA levels (12.4 μg/m³), we estimated a 32% [95% confidence interval (CI): 11, 55] and 41% (95% CI: 14, 74) increase in the incidence of LRI and wLRI, respectively.Conclusion: The findings of this study suggest that infants exposed to FA at an early age have an increased incidence of LRI.     

Formaldehyde induces neurotoxicity to PC12 cells involving inhibition of paraoxonase-1 expression and activity

1. Formaldehyde (FA) has been found to cause toxicity to neurons. However, its neurotoxic mechanisms have not yet been clarified. Increasing evidence has shown that oxidative damage is one of the most critical effects of formaldehyde exposure. Paraoxonase-1 (PON-1) is a pivotal endogenous anti-oxidant. Thus, we hypothesized that FA-mediated downregulation of PON1 is associated with its neurotoxicity. 2. In the present work, we used PC12 cells to study the neurotoxicity of FA and explore whether PON-1 is implicated in FA-induced neurotoxicity. 3. We found that FA has potent cytotoxic and apoptotic effects on PC12 cells. FA induces an accumulation of intracellular reactive oxygen species along with downregulation of Bcl-2 expression, as well as increased cytochrome c release. FA significantly suppressed the expression and activity of PON-1 in PC12 cells. Furthermore, H(2)S, an endogenous anti-oxidant gas, antagonizes FA-induced cytotoxicity as well as 2-hydroxyquinoline, a specific inhibitor of PON-1, which also induces cytotoxicity to PC12 cells. 4. The results of the present study provide, for the first time, evidence that the inhibitory effect on PON-1 expression and activity is involved in the neurotoxicity of FA, and suggest a promising role of PON-1 as a novel therapeutic strategy for FA-mediated toxicity.