Long-lasting effects of tobacco smoking on pulmonary drug-metabolizing enzymes: A case-control study on lung cancer patients

Petruzzelli, Stefano; Camus, Anne-Marie; Carrozzi, Laura; Ghelarducci, L.; M, Rindi; Menconi, G; Angeletti, Carlo Alberto; Ahotupa, Markku; Hietanen, Eino; Aitio, Antero; Saracci, Rodolfo; Bartsch, Helmut; Giuntini, C.

doi:10.1016/0169-5002(89)90282-1

Lung Cancer

1989

DOI: 10.1016/0169-5002(89)90282-1

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Long-lasting effects of tobacco smoking on pulmonary drug-metabolizing enzymes: A case-control study on lung cancer patients

Stefano Petruzzelli

Anne-Marie Camus²,

Laura Carrozzi³

et al.

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Cited by 38 publications

References 40 publications

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Molecular Epidemiology and the Genetics of Environmental Cancer

Shields¹

1991

JAMA

141

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Environmental, occupational, and recreational exposures to carcinogens contribute to cancer risk in humans. Cancer formation is a multistage process involving tumor initiation, promotion, conversion, and progression. Carcinogens can affect any of these stages through genetic and epigenetic mechanisms. The association of a suspected carcinogenic exposure and cancer risk can be studied in populations with classic epidemiologic techniques. However, these techniques are not applicable to the assessment of risk in individuals. Molecular epidemiology, in contrast, is a field that integrates molecular biology, in vitro and in vivo laboratory models, biochemistry, and epidemiology to infer individual cancer risk. Carcinogen-macromolecular adduct levels, and somatic cell mutations can be measured to determine the biologically effective dose of a carcinogen. Molecular epidemiology also explores host cancer susceptibilities, such as carcinogen metabolic activation, DNA repair, endogenous mutation rates, and inheritance of mutated tumor suppressor genes. Substantial interindividual variation for each of these biologic end points has been shown and, therefore, highlights the need for assessing cancer risk on an individual basis. Given the pace of the last decade, it is feasible that the next 10 years will allow molecular epidemiologists to develop a cancer-risk profile for an individual that includes assessment of a number of factors. This will help focus preventive strategies and strengthen quantitative risk assessments.

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Molecular Epidemiology and the Genetics of Environmental Cancer

Shields¹

1991

JAMA

141

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The effect of CYP1A induction on amiodarone disposition in the rat

Elsherbiny

Brocks

2010

Journal of Pharmaceutical Sciences

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Smoking and dietary intake of polycyclic aromatic hydrocarbons as sources of interindividual variability in the baseline excretion of 1-hydroxypyrene in urine

Rooij

Veeger

Bodelier-Bade

et al. 1994

Int. Arch Occup Environ Heath

163

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Seventy-six male volunteers, who were not occupationally exposed to polycyclic aromatic hydrocarbons (PAHs), participated in a study on the effect of tobacco smoking, alcohol consumption, dietary PAH intake, age, and body fat content on the baseline excretion of 1-hydroxypyrene in urine. Major determinants of urinary 1-hydroxypyrene excretion were smoking, dietary PAH intake, and age. The mean 1-hydroxypyrene concentrations in the urine of the volunteers in this study ranged between 0.05 and 0.79 mumol/mol creatinine. Smokers excreted on average 0.25 mumol/mol creatinine (range: 0.10-0.79 mumol/mol creatinine), and nonsmokers on average 0.12 mumol/mol creatinine (range: 0.04-0.29 mumol/mol creatinine). The average number of cigarettes smoked per day correlated well with urinary 1-hydroxypyrene concentrations (rs = 0.67, P < 0.001). The consumption of PAH-containing food products and active smoking account for 99% of total pyrene intake. The effect of age on 1-hydroxypyrene excretion is probably caused by a lower creatinine excretion in the elderly. Passive smoking and fat content had a statistically significant, but negligible effect on urinary 1-hydroxypyrene excretion. Passive smoking and the inhalation of ambient air are relatively in important for total pyrene intake (both account for less than 1%). Neither the consumption of alcohol nor the inhalation of ambient air significantly affected urinary 1-hydroxypyrene excretion. It is concluded that when urinary 1-OH-pyrene excretion is used in the assessment of PAH exposure, one should particularly be aware of the interindividual variability of the baseline excretion of PAH metabolites due to tobacco smoking and dietary PAH intake.

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Long-lasting effects of tobacco smoking on pulmonary drug-metabolizing enzymes: A case-control study on lung cancer patients

Cited by 38 publications

References 40 publications

Molecular Epidemiology and the Genetics of Environmental Cancer

Molecular Epidemiology and the Genetics of Environmental Cancer

The effect of CYP1A induction on amiodarone disposition in the rat

Smoking and dietary intake of polycyclic aromatic hydrocarbons as sources of interindividual variability in the baseline excretion of 1-hydroxypyrene in urine

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