Carcinogens in tobacco smoke: benzo[a]pyrene from Canadian cigarettes and cigarette tobacco.

Kaiserman, Murray; Rickert, W.S.

doi:10.2105/ajph.82.7.1023

Cited by 69 publications

(36 citation statements)

References 4 publications

(1 reference statement)

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“…The levels of PAHs reported in Italian cigarettes in this paper are somewhat lower in comparison with those reported previously (Phillips and Waller, 1991;Kaiserman and Rickert, 1992;Chepiga et al, 2000;Smith et al, 2000). For example, Phillips and Waller (1991) found nearly threefold higher levels of B…”

Section: Discussioncontrasting

confidence: 84%

Sidestream tobacco smoke as the main predictor of exposure to polycyclic aromatic hydrocarbons

Lodovici

Akpan

Evangelisti

et al. 2004

J of Applied Toxicology

114

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Polycyclic aromatic hydrocarbons (PAHs) were measured in mainstream and sidestream tobacco smoke from 14 commercial brands of cigarettes purchased in Italy during 2001-2002. The PAHs detected in smoke and analysed with HPLC and a fluorimetric detector were: fluoranthene, pyrene, benzo[a]anthracene, chrysene, benzo[a]pyrene, benzo[b] fluoranthene, benzo[k] fluoranthene, benzo[g,h,i]perylene and dibenzo[a,h]anthracene. The PAH levels in mainstream smoke from different cigarette brands obtained using an official smoking machine varied by about threefold (from 118 to 374 ng per cigarette for total PAHs and from 23.5 to 100 ng per cigarette for carcinogenic PAHs). Total PAH levels in mainstream smoke were correlated with tar content (r = 0.615, P < 0.05, n = 14). Total PAH content in sidestream smoke, measured by collection of all the smoke produced by a lit cigarette in a glass chamber, was about tenfold higher compared with mainstream smoke. The PAH content in sidestream smoke was relatively uniform (2.3-3.9 and 0.49-1.21 micro g per cigarette for total and carcinogenic PAHs, respectively) and was not correlated with tar content. These results indicate that cigarette manufacturing and filter characteristics influence the PAH composition of mainstream smoke, but have no effect on the PAH content in sidestream smoke, which is the main determinant of smokers' and non-smokers' exposure to PAHs in environmental tobacco smoke.

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Section: Discussioncontrasting

confidence: 84%

Sidestream tobacco smoke as the main predictor of exposure to polycyclic aromatic hydrocarbons

Lodovici

Akpan

Evangelisti

et al. 2004

J of Applied Toxicology

114

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“…Some studies suggest that compared with FM cigarettes, RYO cigarettes yield similar or even higher levels of toxins in smoke (Appel et al, 1990;Kaiserman and Rickert, 1992a;Kaiserman and Rickert, 1992b;Darrall and Figgins, 1998). Moreover, smokers of RYO and FM cigarettes suffer from the same smoking-related diseases (De et al, 1992) and RYO smokers may be at increased risk of particular cancers (e.g.…”

Section: Introductionmentioning

confidence: 99%

CLINICAL STUDY: A comparison of exposure to carcinogens among roll‐your‐own and factory‐made cigarette smokers

2009

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Consumption of roll-your-own (RYO) tobacco is rising but little is known about its in vivo delivery of toxins relative to factory made (FM) cigarettes. To start to address this issue, this study compared the concentrations of metabolites of recognised human carcinogens in smokers of RYO tobacco and FM cigarettes. We opportunistically recruited 127 FM and 28 RYO smokers in central London and collected saliva and urine samples. Saliva samples were assayed for cotinine and urinary samples for 1-HOP and Total NNAL, metabolic markers of polycyclic aromatic hydrocarbons and tobacco-specific Nnitrosamines, respectively. Data on socio-demographic, anthropometric and puffing characteristics were also obtained. Both univariate and multivariate analyses (controlling for age, sex, body mass index, puff flow, puff duration and cotinine) showed no difference in metabolic markers between RYO and FM cigarette smokers. However, significant main effects for cotinine levels and sex were observed in multivariate analyses. Greater levels of cotinine were associated with a greater concentration of both 1-HOP (B=0.002, p=0.037) and NNAL (B=0.002, p<0.001). In addition, women had significantly greater concentrations of urinary 1-HOP (B=0.679, p=0.004) and Total NNAL metabolites (B=0.117, p=0.024) than men, irrespective of the type of cigarettes smoked. More research is now needed to confirm these findings and gender-specific effects in a larger, representative sample. However, results do not support the common belief that roll-your-own cigarettes are less harmful than manufactured cigarettes.

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“…Cadmium has been demonstrated to hinder germinal vesicle breakdown (Fort et al, 2002) and to reduce the percentage of oocytes undergoing normal developmental progression in vivo (Lienesch, Dumont & Bantle, 2000). Interestingly, B[a]P is detected in concentration ranging from 20 to 79ng per cigarette in SS and MS (Kaiserman & Rickert, 1992) and 50-200ng of cadmium is estimated to be inhaled when cigarette is smoked (Elinder, 1985). Both B[a]P and cadmium are much higher in amount in cigarette smoke than 2-ethylpyridine and 3-ethylpyridine, suggesting smoke components tested in this study are more toxic and potent in causing reproductive damages.…”

Section: Discussionmentioning

confidence: 99%

In vitro assessment of reproductive toxicity of cigarette smoke and deleterious consequences of maternal exposure to its constituents

Liu

2012

Biol. Res.

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Cigarette smoke is known to be a serious health risk factor and considered reproductively toxic. In the current study, we investigated whether constituents of cigarette smoke, pyrazine, 2-ethylpyridine, and 3-ethylpyridine, adversely aff ect reproductive functioning such as oocyte maturation and sperm capacitation. Our fi ndings indicated that three smoke components were involved in retardation of oocyte maturation in a dose-dependent manner and the lowest-observed-adverse-eff ect level (LOAEL) was determined to be 10 -10 M. However, individual smoke components administrated at the LOAEL did not attenuate oocyte maturation, demonstrating that all three toxicants were equally required for the observed growth impairment. When exposed to all three components at 10 -10 M during in vitro capacitation, murine sperm lost forward progression and were unable to show adequate hyperactivation, which is indicative of the incompletion of the capacitation process. Only sperm administrated with 3-ethylpyridine alone showed signifi cant reduction in capacitation status, suggesting the chemical is the one responsible for disrupting sperm capacitation. Taken together, this is the fi rst report that documents the eff ect of cigarette smoke components on oocyte maturation and sperm capacitation. The present fi ndings demonstrate the adverse eff ects of smoke constituents of mammalian reproduction and the diff erences in sensitivity to smoke components between male and female gametes. Since both processes take place in the female reproductive system, our data provide new insights into deleterious consequences of maternal exposure to cigarette smoke.

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Carcinogens in tobacco smoke: benzo[a]pyrene from Canadian cigarettes and cigarette tobacco.

Cited by 69 publications

References 4 publications

Sidestream tobacco smoke as the main predictor of exposure to polycyclic aromatic hydrocarbons

Sidestream tobacco smoke as the main predictor of exposure to polycyclic aromatic hydrocarbons

CLINICAL STUDY: A comparison of exposure to carcinogens among roll‐your‐own and factory‐made cigarette smokers

In vitro assessment of reproductive toxicity of cigarette smoke and deleterious consequences of maternal exposure to its constituents

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