Lung cancer among Chinese women

Gao, Yu‐Tang; Blot, William J.; Wang, Zheng; Ershow, Ag G.; Hsu, Cheng Wen; Levin, Lynn I.; Zhang, Rong; Fraumeni, Joseph F.

doi:10.1002/ijc.2910400505

Cited by 373 publications

(230 citation statements)

References 15 publications

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“…Regardless of the accuracy of the estimates, cooking in highly urbanized areas is a major source of acrolein in the atmosphere. Epidemiological findings indicate that emission of acrolein from wok cooking rather than tobacco smoking is linked to the high incidence of lung cancer in Chinese women [31]. A study conducted by Shields and co-workers [32] determined the acrolein emissions from wok cooking to be highest for unrefined Chinese rapeseed oil and lowest for peanut oil.…”

Section: Lipids As a Source Of Acroleinmentioning

confidence: 99%

Acrolein: Sources, metabolism, and biomolecular interactions relevant to human health and disease

Stevens

Maier

2008

Molecular Nutrition Food Res

630

634

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Acrolein (2-propenal) is ubiquitously present in (cooked) foods and in the environment. It is formed from carbohydrates, vegetable oils and animal fats, amino acids during heating of foods, and by combustion of petroleum fuels and biodiesel. Chemical reactions responsible for release of acrolein include heat-induced dehydration of glycerol, retro-aldol cleavage of dehydrated carbohydrates, lipid peroxidation of polyunsaturated fatty acids, and Strecker degradation of methionine and threonine. Smoking of tobacco products equals or exceeds the total human exposure to acrolein from all other sources. The main endogenous sources of acrolein are myeloperoxidase-mediated degradation of threonine and amine oxidase-mediated degradation of spermine and spermidine, which may constitute a significant source of acrolein in situations of oxidative stress and inflammation. Acrolein is metabolized by conjugation with glutathione and excreted in the urine as mercapturic acid metabolites. Acrolein forms Michael adducts with ascorbic acid in vitro, but the biological relevance of this reaction is not clear. The biological effects of acrolein are a consequence of its reactivity towards biological nucleophiles such as guanine in DNA and cysteine, lysine, histidine, and arginine residues in critical regions of nuclear factors, proteases, and other proteins. Acrolein adduction disrupts the function of these biomacromolecules which may result in mutations, altered gene transcription, and modulation of apoptosis.

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Section: Lipids As a Source Of Acroleinmentioning

confidence: 99%

Acrolein: Sources, metabolism, and biomolecular interactions relevant to human health and disease

Stevens

Maier

2008

Molecular Nutrition Food Res

630

634

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“…In all, 31 studies were identified that provided risks of lung cancer stratified by family history of the disease (Tokuhata and Lilienfeld, 1963a, b;Lynch et al, 1982;Ooi et al, 1986;Samet et al, 1986;Gao et al, 1987;Kramer et al, 1987;Sellers et al, 1987;Tsugane et al, 1987;Horwitz et al, 1988;Wu et al, 1988Wu et al, , 1996McDuffie et al, 1989;Wu-Williams et al, 1990;Liu et al, 1991;McDuffie, 1991;Osann, 1991;Shaw et al, 1991;Pavlakou et al, 1993;Schwartz et al, 1996Schwartz et al, , 1999Wang et al, 1996;Brownson et al, 1997;Kreuzer et al, 1998;Mayne et al, 1999;Bromen et al, 2000;Wunsch-Filho et al, 2002;Etzel et al, 2003;Wu et al, 2004;Jin et al, 2005;Matakidou et al, 2005). Three studies (Lynch et al, 1982;Sellers et al, 1987;Schwartz et al, 1999) were excluded from the review as the same data were duplicated in subsequent studies.…”

Section: Case -Control Studiesmentioning

confidence: 99%

Systematic review of the relationship between family history and lung cancer risk

2005

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We performed a systematic review of 28 case -control, 17 cohort and seven twin studies of the relationship between family history and risk of lung cancer and a meta-analysis of risk estimates. Data from both case -control and cohort studies show a significantly increased lung cancer risk associated with having an affected relative. Risk appears to be greater in relatives of cases diagnosed at a young age and in those with multiple affected family members. Increased lung cancer risk was observed in association with an affected spouse and twin studies, while limited, favour shared environmental exposures. The limitations of the currently published epidemiological studies to infer genetic susceptibility are discussed.

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“…[7][8][9] The protective effect of dietary fruit and vegetable in the development of lung cancer has been of considerable interest since it was first described in the 1970s. 10 Recent studies support an effect of total fruit and vegetable intake rather than of individual micronutrients, 11 with the evidence being most consistent for Brassica vegetables, which are rich in isothiocyanates, potent inhibitors of NNK carcinogenesis.…”

mentioning

confidence: 99%

Diet, reproductive factors and lung cancer risk among Chinese women in Singapore: Evidence for a protective effect of soy in nonsmokers

Seow

Poh

Teh

et al. 2001

Intl Journal of Cancer

107

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The factors associated with risk of lung cancer among nonsmokers have not been fully elucidated, but dietary factors have consistently been shown to play a role. Chinese women are unique in having a high incidence of lung cancer despite a low smoking prevalence. This population is also known to have a high intake of soy, a dietary source of phytoestrogens. We conducted a hospital-based case-control study among Singapore Chinese women, comprising 303 cases and 765 age-matched controls, of whom 176 cases and 663 controls were lifetime nonsmokers. Data on demographic background, reproductive factors and dietary intake of fruit, vegetables and soy foods were obtained by in-person interview. We observed an inverse association between intake of total, cruciferous and non-cruciferous vegetables and risk of lung cancer among smokers. Although smokers in the highest tertile of fruit intake also had a lower risk, this was not statistically significant. Higher intake of soy foods significantly reduced risk of lung cancer among lifetime nonsmokers, but not among smokers. When soy isoflavonoid intake in mg/week was computed based on frequency and portion size of intake of eight common local soy foods, the adjusted OR among nonsmokers for the highest tertile compared to the lowest was 0.56, 95% CI 0.37-0.85 (p for trend <0.01). Fruit intake was also significantly associated with reduced lung cancer risk among nonsmokers, but the effect was not significant after adjustment for soy intake. On the other hand, soy intake remained an independent predictor of risk after controlling for fruit intake. Reproductive effects were also primarily confined to lifetime nonsmokers, among whom having 3 or more livebirths (adjusted OR 0.65, 0.44 -0.96) and a menstrual cycle length of more than 30 days (OR 0.46, 0.25-0.84) accorded a significantly reduced risk of lung cancer. Place of birth was significantly associated with risk among nonsmokers (OR 2.6, 1.7-3.9 for China-born vs. local born) but not among smokers. When analysis was restricted to nonsmokers with adenocarcinomas, the dietary effects were consistent or enhanced. On stepwise regression, soy intake and cycle length emerged as the independent dietary and reproductive predictors of lung cancer risk in nonsmokers. These findings are consistent with other evidence suggesting an involvement of estrogen-related pathways in lung cancer among non-smoking women.

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Lung cancer among Chinese women

Cited by 373 publications

References 15 publications

Acrolein: Sources, metabolism, and biomolecular interactions relevant to human health and disease

Acrolein: Sources, metabolism, and biomolecular interactions relevant to human health and disease

Systematic review of the relationship between family history and lung cancer risk

Diet, reproductive factors and lung cancer risk among Chinese women in Singapore: Evidence for a protective effect of soy in nonsmokers

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