Cancer effects of formaldehyde: a proposal for an indoor air guideline value

Nielsen, Gunnar Damgård; Wolkoff, Peder

doi:10.1007/s00204-010-0549-1

Cited by 171 publications

(106 citation statements)

References 103 publications

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“…3,7,19,22 Many institutions and government regulations have considered it to be a carcinogenic agent. 3,5,7,10,11,15,19,22 Although formaldehyde is still needed to prevent microorganism growth (especially fungi), formaldehyde content in the customized embalming fluid described here was almost 80% less than in a conventional formaldehyde mixture. Furthermore, customized specimens provided a less aggressive and contaminated environment than the formaldehyde and cryopreserved specimens.…”

Section: Biohazard Risk and Health Standardsmentioning

confidence: 85%

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Novel embalming solution for neurosurgical simulation in cadavers

Benet

Rincón-Torroella

Lawton

et al. 2014

JNS

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Object Surgical simulation using postmortem human heads is one of the most valid strategies for neurosurgical research and training. The authors customized an embalming formula that provides an optimal retraction profile and lifelike physical properties while preventing microorganism growth and brain decay for neurosurgical simulations in cadavers. They studied the properties of the customized formula and compared its use with the standard postmortem processing techniques: cryopreservation and formaldehyde-based embalming. Methods Eighteen specimens were prepared for neurosurgical simulation: 6 formaldehyde embalmed, 6 cryopreserved, and 6 custom embalmed. The customized formula is a mixture of ethanol 62.4%, glycerol 17%, phenol 10.2%, formaldehyde 2.3%, and water 8.1%. After a standard pterional craniotomy, retraction profiles and brain stiffness were studied using an intracranial pressure transducer and monitor. Preservation time—that is, time that tissue remained in optimal condition—between specimen groups was also compared through periodical reports during a 48-hour simulation. Results The mean (± standard deviation) retraction pressures were highest in the formaldehyde group and lowest in the cryopreserved group. The customized formula provided a mean retraction pressure almost 3 times lower than formaldehyde (36 ± 3 vs 103 ± 14 mm Hg, p < 0.01) and very similar to cryopreservation (24 ± 6 mm Hg, p < 0.01). For research purposes, preservation time in the cryopreserved group was limited to 4 hours and was unlimited for the customized and formaldehyde groups for the duration of the experiment. Conclusions The customized embalming solution described herein is optimal for allowing retraction and surgical maneuverability while preventing decay. The authors were able to significantly lower the formaldehyde content as compared with that in standard formulas. The custom embalming solution has the benefits from both cryopreservation (for example, biological brain tissue properties) and formaldehyde embalming (for example, preservation time and microorganism growth prevention) and minimizes their drawbacks, that is, rapid decay in the former and stiffness in the latter. The presented embalming formula provides an important advance for neurosurgical simulations in research and teaching.

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Section: Biohazard Risk and Health Standardsmentioning

confidence: 85%

“…Additionally, many studies have reported that long-term exposure to high airborne formaldehyde concentrations in the laboratory is hazardous. 6,9,10,11,15 In 2006, the International Agency for Research on Cancer (IARC) 22 and the US Environmental Protection Agency 19 classified formaldehyde as a probable human carcinogen.…”

mentioning

confidence: 99%

Novel embalming solution for neurosurgical simulation in cadavers

Benet

Rincón-Torroella

Lawton

et al. 2014

JNS

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“…48 Nasal epithelia is commonly represented by 75% of columnar surface epithelium, 14% of other epithelial cells, 11% of neutrophils, 0.07% of eosinophils and 0.2% lymphocytes. Apart from the potential value of the nasal epithelial cells for the prediction of cancer risk of the respiratory tract, 16,27 the use of nasal epithelia may allow mechanistic studies of various carcinogens, including those contained in tobacco smoke, 16,39 industrial air pollution, [20][21][22]28 and hair-dyeing.…”

Section: Discussionmentioning

confidence: 99%

Formaldehyde-induced toxicity in the nasal epithelia of workers of a plastic laminate plant

et al. 2016

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Formaldehyde is a ubiquitous volatile organic compound widely used for various industrial purposes. Formaldehyde was reclassified by the International Agency for Research on Cancer as a human carcinogen, based on sufficient evidence for a casual role for nasopharyngeal cancer. However, the mechanisms by which this compound causes nasopharyngeal cancer are not completely understood. Therefore, we have examined the formaldehyde-induced toxicity in the nasal epithelia of the workers of a plastic laminate plant in Bra, Cuneo, Piedmont region, North-Western Italy, hence in the target site for formaldehyderelated nasal carcinogenesis. We have conducted a cross-sectional study aimed at comparing the frequency of 3-(2-deoxy-β-D-erythro-pentafuranosyl)pyrimido[1,2-α]purin-10(3H)-one deoxyguanosine (M 1 dG) adducts, a biomarker of oxidative stress and lipid peroxidation, in 50 male exposed workers and 45 male controls using 32 P-DNA post-labeling. The personal levels of formaldehyde exposure were analysed by gas-chromatography mass-spectrometry. The smoking status was estimated by measuring the concentrations of urinary cotinine by gas-chromatography mass-spectrometry. The air monitoring results showed that the exposure levels of formaldehyde were significantly greater for the plastic laminate plant workers, 211.4 ± 14.8 standard error (SE) µg m −3 , than controls, 35.2 ± 3.4 (SE) µg m −3 , P < 0.001. The levels of urinary cotinine were 1064 ± 118 ng ml −1 and 14.18 ± 2.5 ng ml −1 in smokers and non-smokers, respectively, P < 0.001. The M 1 dG adduct frequency per 10 8 normal nucleotides was significantly higher among the workers of the plastic laminate plant exposed to formaldehyde, 111.6 ± 14.3 (SE), compared to controls, 49.6 ± 3.4 (SE), P < 0.001. This significant association persisted also when personal dosimeters were used to measure the extent of indoor levels of formaldehyde exposure. No influences of smoking and age were observed across the study population. However, after categorization for occupational exposure, a significant effect was found in the controls, P = 0.018, where the levels of DNA damage were significantly correlated with the levels of urinary cotinine, regression coefficient (β) = 0.494 ± 0.000 (SE), P < 0.002. Our findings indicated that M 1 dG adducts constitute a potential mechanism of formaldehydeinduced toxicity. Persistent DNA damage contributes to the general decline of the physiological mechanisms designed to maintain cellular homeostasis.

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“…Nitrogen oxides (particularly NO, NO 2 , and N 2 O 3 ) in tobacco smoke can be anticipated to contribute to enhanced protein nitrosylation (S-nitrosylation), a key post-translation modification that frequently targets apoptotic and prosurvival proteins such as Ras, caspases, and IKKb (1, 2). Cigarette smoke also contains oxidants (including formaldehyde) that are implicated in carcinogenesis (33,34).…”

Section: Discussionmentioning

confidence: 99%

S-Nitrosoglutathione Reductase in Human Lung Cancer

Marozkina¹,

Wei

Yemen³

et al. 2012

Am J Respir Cell Mol Biol

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S-Nitrosoglutathione (GSNO) reductase regulates cell signaling pathways relevant to asthma and protects cells from nitrosative stress. Recent evidence suggests that this enzyme may prevent human hepatocellular carcinoma arising in the setting of chronic hepatitis. We hypothesized that GSNO reductase may also protect the lung against potentially carcinogenic reactions associated with nitrosative stress. We report that wild-type Ras is S-nitrosylated and activated by nitrosative stress and that it is denitrosylated by GSNO reductase. In human lung cancer, the activity and expression of GSNO reductase are decreased. Further, the distribution of the enzyme (including its colocalization with wild-type Ras) is abnormal. We conclude that decreased activity of GSNO reductase could leave the human lung vulnerable to the oncogenic effects of nitrosative stress, as is the case in the liver. This potential should be considered when developing therapies that inhibit pulmonary GSNO reductase to treat asthma and other conditions. Keywords: lung cancer; S-nitrosoglutathione reductase; Ras Protein S-nitrosylation, the post-translational modification of a cysteine by the attachment of an NO group, is a regulated pathway that is responsible for a variety of signaling effects (1, 2). S-nitrosylation, caused both by exposure to exogenous nitrogen oxides and by the activity of nitric oxide synthase (NOS), is involved in the regulation of gene expression, cell division, and a spectrum of other processes in cell biology. For example, the S-nitrosylation of wild-type Ras by endothelial NOS (eNOS) is required for cell proliferation and tumor growth in a common model of tumorigenesis (3). Specifically, oncogenic K-Ras-GTP activates proteins to initiate human tumor growth. Of these proteins, only the phosphatidylinositol 3 kinase (PI3 kinase)/Akt pathway is indispensable for tumor maintenance (3). The essential Akt substrate for this process is eNOS. The activation of NOS, in turn, S-nitrosylates and activates wild-type (wt) H-Ras and N-Ras proteins at cysteine 118. Either the knockdown of eNOS or the mutation of wt Ras cysteine 118 (the site of S-nitrosylation) prevents the activation of Ras and the formation of tumors (3).Although the activation of NOS leads to wt Ras S-nitrosylation, the mechanism by which Ras can be denitrosylated is not known. As with phosphorylation/dephosphorylation coupling, the addition and removal of NO from cysteines are normally regulated in cell biology, and several enzymes serve as denitrosylases (1, 2, 4, 5). In the human airway, S-nitrosoglutathione (GSNO) reductase is an important enzyme responsible for denitrosylation (1,4,6,7). This highly conserved enzyme is traditionally regarded as an aldehyde dehydrogenase, although it is somewhat more efficient as GSNO reductase (5,8,9). Its relative redox activities depend on substrate concentration and the local nicotinamide adenine dinucleotide/ nicotinamide adenine dinucleotide reduced (NAD 1 /NADH) ratio. Our evidence suggests that decreased activity of GSNO re...

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Cancer effects of formaldehyde: a proposal for an indoor air guideline value

Cited by 171 publications

References 103 publications

Novel embalming solution for neurosurgical simulation in cadavers

Novel embalming solution for neurosurgical simulation in cadavers

Formaldehyde-induced toxicity in the nasal epithelia of workers of a plastic laminate plant

S-Nitrosoglutathione Reductase in Human Lung Cancer

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