Environmental and genetic risk factors and gene-environment interactions in the pathogenesis of chronic obstructive lung disease.

Walter, Robert; Gottlieb, Daniel J.; O’Connor, George T.

doi:10.1289/ehp.00108s4733

Cited by 46 publications

(19 citation statements)

References 205 publications

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“…In this study, pear intake significantly reduced the odds of being in the high 1-OHP group (Table III). Since air pollutants including PAHs, are risk factors for both COPD and lung cancer [Walter et al, 2000;Cohen, 2000], our observation that pear intake reduced urinary 1-OHP levels suggests the chemopreventive potential of pear consumption via reduction of bioactive intermediates of PAHs. No association was found between the urinary 1-OHP levels and the consumption of several foods that contain high levels of benzo[a]pyrene [Kazerouni et al, 2002], such as steak, grilled fish, and beef/pork barbecue.…”

Section: Factors That Reduce Pah Exposurementioning

confidence: 87%

Sources of polycyclic aromatic hydrocarbon exposure in non‐occupationally exposed Koreans

Yang

Kim

Lee

et al. 2003

Environ and Mol Mutagen

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Urinary 1-hydroxypyrene (1-OHP), an exposure biomarker for polycyclic aromatic hydrocarbons (PAHs), was used to identify potential sources of PAH exposure for 660 Koreans who were not occupationally exposed to PAHs (65% male; 35% female; mean age, 36.5 Ϯ 11.1 years). In this study, 74% of subjects had detectable levels of urinary 1-OHP, with a concentration range of 0.001-3.796 g/L (median, 0.079 g/L). A backward elimination was conducted: five variables were selected with a significance level for removal of P Յ 0.1. The results of this study showed that residence in areas with relatively poor environmental conditions (Seoul and Suwon) was strongly associated with high concentrations of urinary 1-OHP (P ϭ 0.007), while consumption of fried chicken and length of time spent outdoors had marginal positive associations with urinary 1-OHP levels (P ϭ 0.06 and P ϭ 0.09, respectively). Compared with the above three factors, tobacco smoking and urinary cotinine levels were poorly associated with urinary 1-OHP (P ϭ 0.16 and 0.23, respectively). Pear consumption had an inverse association with urinary 1-OHP levels (P Ͻ 0.01). Individual variations in urinary 1-OHP concentrations were evaluated by considering the subjects' age, sex, and genetic polymorphisms in enzymes involved in the metabolism of PAHs. Among the individual variations, GSTT1-present subjects showed higher 1-OHP levels than GSTT1-absent subjects in cities having 10-m particulate matter (PM 10 ) levels and population density lower than those of Seoul and Suwon (P Ͻ 0.05). These epidemiological results suggest that the above factors that should be considered in preventing PAH exposure. Environ. Mol. Mutagen. 42:250-257, 2003.

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Section: Factors That Reduce Pah Exposurementioning

confidence: 87%

Sources of polycyclic aromatic hydrocarbon exposure in non‐occupationally exposed Koreans

Yang

Kim

Lee

et al. 2003

Environ and Mol Mutagen

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“…The interaction between two phase II deficient enzymes (GSTT1 null and GSTP1 Val) or a phase I hyperactive enzyme (CYP1A1 2A) and a phase II absent enzyme (GSTT1 null) results in a larger amount of toxic compounds that might have a role in the initiation or progression of COPD (Rebbeck, 1997;Indulski and Lutz, 2000;Watson et al, 1998;Walter et al, 2000).…”

Section: Discussionmentioning

confidence: 99%

CYP1A1, CYP2E1, GSTM1, GSTT1, GSTP1, and TP53 polymorphisms: do they indicate susceptibility to chronic obstructive pulmonary disease and non-small-cell lung cancer?

et al. 2004

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Gene polymorphisms of phase I (CYP1A1 and CYP2E of cytochrome P,) and phase II (GSTM1, GSTT1 and GSTP1 of glutathione-S-transferase,) enzymes and the TP53 tumor suppressor gene were studied as markers in a sample of 262 Brazilians of European descent, the sample consisting of 97 patients with non-small-cell lung cancer (NSCLC), 75 patients with chronic obstructive pulmonary disease (COPD) and 90 control individuals. For NSCLC, we found no significant relationship between any of the markers studied and susceptibility to this disease. With respect to COPD, although the distribution of the CYP1A1, GSTM1, GSTP1, GSTT1 and TP53 genotypes was similar to that of the controls the frequency of the CYP2E1*1A/*5B heterozygote was about 6 times higher in COPD patients than in controls (OR= 6.3; CI = 1.1-35.5 for p = 0.04). Individuals who presented the GSTT1 null phenotype and GSTP1 Ile/Val genotype had a risk about four times higher (OR= 4.0; CI = 1.2-14.6 for p = 0.02) of having COPD than individuals without these genotypes, the same being true for individuals having the GSTT1 null phenotype and CYP1A1*1A/*2A genotype (OR= 3.7; 1.1-14.6 for p = 0.04).These results suggest that the CYP2E1 and GSTT1 + GSTP or GSTT1 + CYP1A1 polymorphisms may be predictive of susceptibility to COPD, at least in this population of European ancestry.

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“…Recently, as a result of the excellent sensitivity and specificity of GM-CSF autoantibody assays in identifying this form of PAP [3], it has been proposed that the nomenclature for this condition should be changed to ''autoimmune PAP'' rather than ''idiopathic PAP'' [4]. Secondary or hereditary PAP is not associated with GM-CSF autoantibodies but develops as a consequence of a separate underlying disorder or genetic background [5]. Recently, we demonstrated that the characteristic high-resolution computed tomography (HRCT) findings in secondary PAP are distinct from those in autoimmune PAP [6].…”

Section: To the Editorsmentioning

confidence: 99%

Subsequent COPD and lung cancer in patients with autoimmune disease: Table 1–

Hemminki¹,

Liu²,

Ji³

et al. 2011

Eur Respir J

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Environmental and genetic risk factors and gene-environment interactions in the pathogenesis of chronic obstructive lung disease.

Cited by 46 publications

References 205 publications

Sources of polycyclic aromatic hydrocarbon exposure in non‐occupationally exposed Koreans

Sources of polycyclic aromatic hydrocarbon exposure in non‐occupationally exposed Koreans

CYP1A1, CYP2E1, GSTM1, GSTT1, GSTP1, and TP53 polymorphisms: do they indicate susceptibility to chronic obstructive pulmonary disease and non-small-cell lung cancer?

Subsequent COPD and lung cancer in patients with autoimmune disease: Table 1–

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