Assessment of lipid peroxidation and p53 as a biomarker of carcinogenesis among workers exposed to formaldehyde in the cosmetic industry

Attia, Dalia Ismail; Mansour, Neveen; Taha, Fatma; Dein, Aisha Seif El

doi:10.1177/0748233714547152

Cited by 15 publications

(11 citation statements)

References 37 publications

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“…We have excluded new occupational studies that do not include measured FA concentrations, studies where the exposure–response relationships could not be evaluated (e.g. Attia et al 2014; Santovito et al 2014), and studies with complex environmental exposures (e.g. Vilavert et al 2014) where no measured health effect was included or where a low-level environmental FA exposure was a proxy of an exposure to a complex outdoor air mixture (e.g.…”

Section: Introductionmentioning

confidence: 99%

Re-evaluation of the WHO (2010) formaldehyde indoor air quality guideline for cancer risk assessment

2016

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In 2010, the World Health Organization (WHO) established an indoor air quality guideline for short- and long-term exposures to formaldehyde (FA) of 0.1 mg/m3 (0.08 ppm) for all 30-min periods at lifelong exposure. This guideline was supported by studies from 2010 to 2013. Since 2013, new key studies have been published and key cancer cohorts have been updated, which we have evaluated and compared with the WHO guideline. FA is genotoxic, causing DNA adduct formation, and has a clastogenic effect; exposure–response relationships were nonlinear. Relevant genetic polymorphisms were not identified. Normal indoor air FA concentrations do not pass beyond the respiratory epithelium, and therefore FA’s direct effects are limited to portal-of-entry effects. However, systemic effects have been observed in rats and mice, which may be due to secondary effects as airway inflammation and (sensory) irritation of eyes and the upper airways, which inter alia decreases respiratory ventilation. Both secondary effects are prevented at the guideline level. Nasopharyngeal cancer and leukaemia were observed inconsistently among studies; new updates of the US National Cancer Institute (NCI) cohort confirmed that the relative risk was not increased with mean FA exposures below 1 ppm and peak exposures below 4 ppm. Hodgkin’s lymphoma, not observed in the other studies reviewed and not considered FA dependent, was increased in the NCI cohort at a mean concentration ≥0.6 mg/m3 and at peak exposures ≥2.5 mg/m3; both levels are above the WHO guideline. Overall, the credibility of the WHO guideline has not been challenged by new studies.

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Section: Introductionmentioning

confidence: 99%

Re-evaluation of the WHO (2010) formaldehyde indoor air quality guideline for cancer risk assessment

2016

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“…However, it may not be necessary to control for menstrual cycle given the lack of impact of circulating sex hormones on wave reflection and pulse wave velocity (Voges et al, 2012). While it is enticing to monitor plasma FA, FA has a half-time of only 1-1.5 minutes in plasma (Wold Health Organization, 1987), making monitoring of FA metabolites, such as formate salts in the urine, the next best option (Attia et al, 2016), despite levels of detection of formate being questionable during relatively low levels of FA exposure (Boeniger, 1987).…”

Section: Experimental Considerationsmentioning

confidence: 99%

Arterial stiffness and carotid distensibility following acute formaldehyde exposure in female adults

et al. 2021

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Formaldehyde (FA) is a ubiquitous organic preservative used in several industries and represents an occupational health hazard. Short-term exposure to FA can increase oxidative stress and cause a decrease in conduit vessel function. These decrements in vascular function may extend to the arterial architecture, predisposing individuals to increased risk of cardiovascular disease. The purpose of this study was to investigate the impact of an acute 90-minute FA exposure period (259 ± 95 ppb) on indices of arterial architecture. Arterial stiffness and carotid distensibility as determined by central pressures, augmentation index (AIx), and carotid-femoral pulse wave velocity (cfPWV) ( n=13F, 24 ± 1 year) as well as carotid stiffness and intima media thickness (IMT) ( n = 9F, 23 ± 1 year) were assessed prior to (Pre-FA) and immediately following (Post-FA) exposure to FA in human cadaver dissection laboratories. Central pressures and cfPWV (Pre-FA: 5.2 ± 0.8 m.s−1, Post-FA: 5.2 ± 1.1 m s−1) were unchanged by acute FA exposure ( p > 0.05). Carotid stiffness parameters and distension were unchanged by acute FA exposure ( p > 0.05), although distensibility (Pre-FA: 33.9 ± 10.5[10–3*kPa−1], Post-FA: 25.9 ± 5.5[10–3*kPa-1], p < 0.05), and IMT (Pre-FA: 0.42 ± 0.05 mm, Post-FA: 0.51 ± 0.11 mm, p < 0.05) decreased and increased, respectively. Individual Pre- to Post-FA changes in these markers of arterial architecture did not correlate with levels of FA exposure ([FA]: 20–473 ppb) ( p > 0.05). Our group previously found vascular function decrements following acute FA exposure in human cadaver laboratories; here we found that carotid distensibility and intima media thickness are altered following FA exposure.

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“…According to IARC, there is robust evidence of a causal link between FA exposure and the risk of nasopharyngeal cancer and leukemia [ 20 , 21 ]. Indeed, FA exposure and the oxidative stress it induces are cytotoxic and potentially carcinogenic [ 22 ].…”

Section: Introductionmentioning

confidence: 99%

Formaldehyde Crosses the Human Placenta and Affects Human Trophoblast Differentiation and Hormonal Functions

et al. 2015

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The chorionic villus of the human placenta is the source of specific endocrine functions and nutrient exchanges. These activities are ensured by the syncytiotrophobast (ST), which bathes in maternal blood. The ST arises and regenerates throughout pregnancy by fusion of underlying cytotrophoblasts (CT). Any anomaly of ST formation or regeneration can affect pregnancy outcome and fetal growth. Because of its direct interaction with maternal blood, the ST is sensitive to drugs, pollutants and xenohormones. Ex vivo assays of perfused cotyledon show that formaldehyde, a common pollutant present in furniture, paint and plastics, can accumulate in the human placenta and cross to the fetal compartment. By means of RT-qPCR, immunoblot and immunocytochemistry experiments, we demonstrate in vitro that formaldehyde exerts endocrine toxicity on human trophoblasts, including a decrease in the production of protein hormones of pregnancy. In addition, formaldehyde exposure triggered human trophoblast fusion by upregulating syncitin-1 receptor expression (ASC-type amino-acid transporter 2: ASCT2). Moreover, we show that formaldehyde-exposed trophoblasts present an altered redox status associated with oxidative stress, and an increase in ASCT2 expression intended to compensate for this stress. Finally, we demonstrate that the adverse effects of formaldehyde on trophoblast differentiation and fusion are reversed by N-acetyl-L-cysteine (Nac), an antioxidant.

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Assessment of lipid peroxidation and p53 as a biomarker of carcinogenesis among workers exposed to formaldehyde in the cosmetic industry

Cited by 15 publications

References 37 publications

Re-evaluation of the WHO (2010) formaldehyde indoor air quality guideline for cancer risk assessment

Re-evaluation of the WHO (2010) formaldehyde indoor air quality guideline for cancer risk assessment

Arterial stiffness and carotid distensibility following acute formaldehyde exposure in female adults

Formaldehyde Crosses the Human Placenta and Affects Human Trophoblast Differentiation and Hormonal Functions

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