Acrylamide levels in smoke from conventional cigarettes and heated tobacco products and exposure assessment in habitual smokers

Esposito, Francesco; Squillante, Jonathan; Nolasco, Agata; Montuori, Paolo; Macrì, Pasquale Giuseppe; Cirillo, Teresa

doi:10.1016/j.envres.2021.112659

Cited by 20 publications

(14 citation statements)

References 50 publications

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“…AA, GL, and ACA are shown to be present in different foods (GL; , AA; − ACA). AA and GL are also components of tobacco smoke. − GL and AA are classified as probable carcinogens to humans (group 2A) by the International Agency for Research on Cancer, and ACA has been considered not classifiable as to its carcinogenicity to humans (group 3) . These electrophiles could possibly be metabolized to GLA.…”

Section: Resultsmentioning

confidence: 99%

Pathways to Identify Electrophiles In Vivo Using Hemoglobin Adducts: Hydroxypropanoic Acid Valine Adduct and Its Possible Precursors

Vryonidis

Karlsson

Aasa

et al. 2022

Chem. Res. Toxicol.

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Analytical methods and tools for the characterization of the human exposome by untargeted mass spectrometry approaches are advancing rapidly. Adductomics methods have been developed for untargeted screening of short-lived electrophiles, in the form of adducts to proteins or DNA, in vivo. The identification of an adduct and its precursor electrophile in the blood is more complex than that of stable chemicals. The present work aims to illustrate procedures for the identification of an adduct to N-terminal valine in hemoglobin detected with adductomics, and pathways for the tracing of its precursor and possible exposure sources. Identification of the adduct proceeded via preparation and characterization of standards of adduct analytes. Possible precursor(s) and exposure sources were investigated by measurements in blood of adduct formation by precursors in vitro and adduct levels in vivo. The adduct was identified as hydroxypropanoic acid valine (HPA-Val) by verification with a synthesized reference. The HPA-Val was measured together with other adducts (from acrylamide, glycidamide, glycidol, and acrylic acid) in human blood (n = 51, schoolchildren). The HPA-Val levels ranged between 6 and 76 pmol/g hemoglobin. The analysis of reference samples from humans and rodents showed that the HPA-Val adduct was observed in all studied samples. No correlation of the HPA-Val level with the other studied adducts was observed in humans, nor was an increase in tobacco smokers observed. A small increase was observed in rodents exposed to glycidol. The formation of the HPA-Val adduct upon incubation of blood with glycidic acid (an epoxide) was shown. The relatively high adduct levels observed in vivo in relation to the measured reactivity of the epoxide, and the fact that the epoxide is not described as naturally occurring, suggest that glycidic acid is not the only precursor of the HPA-Val adduct identified in vivo. Another endogenous electrophile is suspected to contribute to the in vivo HPA-Val adduct level.

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Section: Resultsmentioning

confidence: 99%

Pathways to Identify Electrophiles In Vivo Using Hemoglobin Adducts: Hydroxypropanoic Acid Valine Adduct and Its Possible Precursors

Vryonidis

Karlsson

Aasa

et al. 2022

Chem. Res. Toxicol.

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“…Moreover, although the FFQ refers to the previous year, dietary habits have been shown to remain fairly stable over time [ 61 ]; (iii) the number of foods considered in the dietary exposure to acrylamide was higher than most previous studies [ 19 , 22 , 23 , 24 , 25 ], including typical foods in Spain such as churros or polvorones. For these reasons, we consider that the estimate of dietary acrylamide should be very close to what is ingested by our population; and (iv) for estimation of acrylamide from cigarette smoking, we considered the different types and brands of cigarettes [ 45 ].…”

Section: Discussionmentioning

confidence: 99%

“…Data on smoking status (never, former, or current smoker), years of smoking, and average number of cigarettes per day were considered for former and current smokers. The acrylamide from cigarette smoking (µg/day) was calculated by multiplying the average number of cigarettes per day by the average amount of acrylamide contained in each cigarette (566 ng/cigarette) according to Esposito et al [ 45 ]. They randomly selected 65 conventional cigarettes in Italy, including different brands and types of cigarettes.…”

Section: Methodsmentioning

confidence: 99%

Dietary and Smoking Acrylamide and Prostate Cancer Risk: CAPLIFE Study

Lozano-Lorca,

Muñoz-Bravo,

Barrios-Rodríguez

et al. 2024

Nutrients

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Acrylamide is a probable carcinogen. Its main sources are the diet and tobacco. The association between acrylamide intake from the diet and tobacco and prostate cancer (PCa) has not been previously evaluated. We aimed to evaluate the relationship between dietary acrylamide intake and exposure to acrylamide through cigarettes and PCa risk. A population-based case–control (CAPLIFE) study was conducted, including 428 incident PCa cases and 393 controls. Smoking and dietary information, with a validated food frequency questionnaire, was collected. We calculated the amount of acrylamide from both sources, and tertiles (Ts) were created. Multivariable logistic regression and restricted cubic spline models were applied to assess the association between exposure to acrylamide and PCa risk. The median was similar for acrylamide in both dietary and smoking acrylamide among PCa cases and controls. No association was observed between dietary acrylamide intake and overall PCa risk (adjusted ORT3vsT1 = 0.90 (95% CI 0.59, 1.37)). A risk trend was observed for acrylamide exposure from cigarette smoking (p-trend = 0.032), with the highest odds in those subjects with the high exposure to acrylamide through cigarettes (adjusted ORT3vsT1 = 1.67 (95% CI 0.92, 3.04)). The restricted cubic splines suggested a linear relationship. In conclusion, acrylamide from smoking could be positively associated with PCa risk, but no association was observed for dietary acrylamide.

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“…Furthermore, AA is formed through a thermal process during the Maillard reaction of carbohydrate-rich foods or tobaccos. 1,2 As a hydrophilic and low molecular weight chemical, AA can be absorbed via ingestion, inhalation, and dermal contact and is subsequently metabolically activated by cytochrome P450 2E1 (CYP2E1) to form glycidamide (GA); GA is recognized as an activated metabolite with higher carcinogenic activity than that of AA. This carcinogenic activity is due to its covalent interaction with DNA strands.…”

Section: Introductionmentioning

confidence: 99%

Acrylamide-induced meiotic arrest of spermatocytes in adolescent mice by triggering excessive DNA strand breaks: Potential therapeutic effects of resveratrol

et al. 2023

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Background: Baked carbohydrate-rich foods are the main source of acrylamide (AA) in the general population and are widely consumed by teenagers. Considering the crucial development of the reproductive system during puberty, the health risks posed by AA in adolescent males have raised public concern. Methods: In this study, we exposed 3-week-old male pubertal mice to AA for 4 weeks to evaluate its effect on spermatogenesis using computer-assisted sperm analysis (CASA) and historical analysis. Flow cytometric analysis and meiocyte spreading assay were conducted to assess meiosis in mice. The expression of meiosis-related proteins and double-strand break (DSB) proteins were evaluated by immunoblot analyses. Additionally, isolated spermatocytes were used to explore the role of resveratrol in AA-induced damages of meiosis. Results: Our results showed that AA decreased the testicular and epididymal indexes, reduced sperm count and motility, and induced morphological disruption of the testes in pubertal mice. Subsequent meiotic analysis revealed that AA increased the proportion of 4C spermatocytes and decreased the proportion of 1C spermatids. The expression levels of meiosis-related proteins (SYCP3, Cyclin A1 and CDK2) were downregulated, and signaling proteins (γH2AX, p-CHK2 and p-ATM) expression levels were upregulated in AA-treated mice testes. Similar expression patterns were observed in primary spermatocytes treated with AA and these effects were reversed significantly by resveratrol. Conclusions: Our results indicate that AA induces meiotic arrest via persistent activation of DSBs, which may contribute to AA-compromised spermatogenesis. Resveratrol could serve as a potential therapeutic agent against AA-induced meiotic toxicity. These data highlight the importance of natural product supplementation for treating AA-related reproductive toxicity.

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Acrylamide levels in smoke from conventional cigarettes and heated tobacco products and exposure assessment in habitual smokers

Cited by 20 publications

References 50 publications

Pathways to Identify Electrophiles In Vivo Using Hemoglobin Adducts: Hydroxypropanoic Acid Valine Adduct and Its Possible Precursors

Pathways to Identify Electrophiles In Vivo Using Hemoglobin Adducts: Hydroxypropanoic Acid Valine Adduct and Its Possible Precursors

Dietary and Smoking Acrylamide and Prostate Cancer Risk: CAPLIFE Study

Acrylamide-induced meiotic arrest of spermatocytes in adolescent mice by triggering excessive DNA strand breaks: Potential therapeutic effects of resveratrol

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