Association of PAH-DNA adducts in peripheral white blood cells with dietary exposure to polyaromatic hydrocarbons.

Rothman, Nathaniel; Poirier, Miriam C.; Haas, Robert A.; Correa‐Villaseñor, Adolfo; Ford, Patrick D.; Hansen, John A.; O’Toole, Tara; Strickland, Paul T.

doi:10.1289/ehp.9399265

Cited by 44 publications

(26 citation statements)

References 7 publications

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“…Previous studies have reported that consumption of processed or cured meat and meat products is positively associated with the formation of PAH-DNA adducts (48,49) . It has been found that individuals who consumed barbecued food more than twice in the previous 2 weeks had fourfold increased risk of having elevated adducts level compared with individuals consuming the food two or fewer times (41) .…”

Section: Discussionmentioning

confidence: 99%

Impact of prenatal exposure to polycyclic aromatic hydrocarbons from maternal diet on birth outcomes: a birth cohort study in Korea

Lamichhane¹,

Leem²,

Kim³

et al. 2016

Public Health Nutr.

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Objective: Polycyclic aromatic hydrocarbons (PAH) are common dietary exposures that cross the human placenta and are classified as a probable human carcinogen. The aim of the present study was to investigate the potential impact of exposure to PAH-containing meat consumed during pregnancy on birth outcomes. Design: Prospective birth cohort study. Only non-smoking women with singleton pregnancies, who were free from chronic disease such as diabetes and hypertension, were included in the study. Maternal consumption of PAH-rich meat was estimated through FFQ. Multiple linear regression was used to assess factors related to higher intake and the association between dietary PAH and birth outcomes.

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Section: Discussionmentioning

confidence: 99%

Impact of prenatal exposure to polycyclic aromatic hydrocarbons from maternal diet on birth outcomes: a birth cohort study in Korea

Lamichhane¹,

Leem²,

Kim³

et al. 2016

Public Health Nutr.

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“…Also, it will help to identify variables that should be considered as potential confounders in studies of PAH-DNA adducts and breast cancer. Other studies that have examined contributors to PAH-DNA adduct formation have either been feeding studies (Rothman et al, 1990;Kang et al, 1995), or have used highly exposed occupational cohorts (Rothman et al, 1993b;Tuominen et al, 2002). In addition, the only other population-based investigations have been limited by small sample sizes (Scherer et al, 2000;Georgiadis et al, 2001).…”

Section: Discussionmentioning

confidence: 99%

“…They have most frequently been studied in populations with high occupational exposure, such as firefighters (Rothman et al, 1993a;Rothman et al, 1993b); and coke oven, aluminum, and foundry workers (Mastrangelo et al, 1996). Nonoccupational exposure sources include tobacco smoke (Besarati et al, 2002); foods such as charred, smoked, and broiled meats and leafy vegetables (Phillips, 1999); indoor contamination (Lewis et al, 1999); and air pollution (Lioy and Greenberg, 1990).…”

Section: Introductionmentioning

confidence: 99%

Residential environmental exposures and other characteristics associated with detectable PAH-DNA adducts in peripheral mononuclear cells in a population-based sample of adult females

Shantakumar

Gammon

Eng

et al. 2005

J Expo Sci Environ Epidemiol

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The detection of polycyclic aromatic hydrocarbon (PAH)-DNA adducts in human lymphocytes may be useful as a surrogate end point for individual cancer risk prediction. In this study, we examined the relationship between environmental sources of residential PAH, as well as other potential factors that may confound their association with cancer risk, and the detection of PAH-DNA adducts in a large population-based sample of adult women. Adult female residents of Long Island, New York, aged at least 20 years were identified from the general population between August 1996 and July 1997. Among 1556 women who completed a structured questionnaire, 941 donated sufficient blood (25 þ ml) to allow use of a competitive ELISA for measurement of PAH-DNA adducts in peripheral blood mononuclear cells. Ambient PAH exposure at the current residence was estimated using geographic modeling (n ¼ 796). Environmental home samples of dust (n ¼ 356) and soil (n ¼ 360) were collected on a random subset of long-term residents (15 þ years). Multivariable regression was conducted to obtain the best-fitting predictive models. Three separate models were constructed based on data from : (A) the questionnaire, including a dietary history; (B) environmental home samples; and (C) geographic modeling. Women who donated blood in summer and fall had increased odds of detectable PAH-DNA adducts (OR ¼ 2.65, 95% confidence interval (CI) ¼ 1.69, 4.17; OR ¼ 1.59, 95% CI ¼ 1.08, 2.32, respectively), as did current and past smokers (OR ¼ 1.50, 95% CI ¼ 1.00, 2.24; OR ¼ 1.46, 95% CI ¼ 1.05, 2.02, respectively). There were inconsistent associations between detectable PAH-DNA adducts and other known sources of residential PAH, such as grilled and smoked foods, or a summary measure of total dietary benzo-[a]-pyrene (BaP) intake during the year prior to the interview. Detectable PAH-DNA adducts were inversely associated with increased BaP levels in dust in the home, but positively associated with BaP levels in soil outside of the home, although CIs were wide. Ambient BaP estimates from the geographic model were not associated with detectable PAH-DNA adducts. These data suggest that PAH-DNA adducts detected in a population-based sample of adult women with ambient exposure levels reflect some key residential PAH exposure sources assessed in this study, such as cigarette smoking.

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“…In a study among roofers, PAH-DNA adduct levels in WBC correlated with the amount of PAH in skin wipes, but not with the amount of PAH in personal air samples, indicating that dermal contact might be a major route for DNA adduct formation in WBC (Herbert et al, 1990). Furthermore, several studies showed that the consumption of PAH-containing foods significantly enhanced DNA adduct levels in peripheral blood lymphocytes (Rothman et al, 1993a(Rothman et al, , 1993bVan Maanen et al, 1994b). The possibility for multiple routes of exposure may further complicate the relationship between adduct levels in target tissues and surrogate tissues.…”

Section: Studies In Humansmentioning

confidence: 99%

A Critical Evaluation of DNA Adducts as Biological Markers for Human Exposure to Polycyclic Aromatic Compounds

Godschalk¹,

Schooten²,

Bartsch³

2003

BMB Reports

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The causative role of polycyclic aromatic hydrocarbons (PAH) in human carcinogenesis is undisputed. Measurements of PAH-DNA adduct levels in easily accessible white blood cells therefore represent useful early endpoints in exposure intervention or chemoprevention studies. The successful applicability of DNA adducts as early endpoints depends on several criteria: i. adduct levels in easily accessible surrogate tissues should reflect adduct levels in target-tissues, ii. toxicokinetics and the temporal relevance should be properly defined. iii. sources of interand intra-individual variability must be known and controllable, and finally iv. adduct analyses must have advantages as compared to other markers of PAHexposure. In general, higher DNA adduct levels or a higher proportion of subjects with detectable DNA adduct levels were found in exposed individuals as compared with nonexposed subjects, but saturation may occur at high exposures. Furthermore, DNA adduct levels varied according to changes in exposure, for example smoking cessation resulted in lower DNA adduct levels and adduct levels paralleled seasonal variations of air-pollution. Intraindividual variation during continuous exposure was low over a short period of time (weeks), but varied significantly when longer time periods (months) were investigated. Inter-individual variation is currently only partly explained by genetic polymorphisms in genes involved in PAH-metabolism and deserves further investigation. DNA adduct measurements may have three advantages over traditional exposure assessment: i. they can smooth the extreme variability in exposure which is typical for environmental toxicants and may integrate exposure over a longer period of time. Therefore, DNA adduct assessment may reduce the monitoring effort. ii. biological monitoring of DNA adducts accounts for all exposure routes. iii. DNA adducts may account for inter-individual differences in uptake, elimination, distribution, metabolism and repair amongst exposed individuals. In conclusion, there is now a sufficiently large scientific basis to justify the application of DNA adduct measurements as biomarkers in exposure assessment and intervention studies. Their use in risk-assessment, however, requires further investigation.

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Association of PAH-DNA adducts in peripheral white blood cells with dietary exposure to polyaromatic hydrocarbons.

Cited by 44 publications

References 7 publications

Impact of prenatal exposure to polycyclic aromatic hydrocarbons from maternal diet on birth outcomes: a birth cohort study in Korea

Impact of prenatal exposure to polycyclic aromatic hydrocarbons from maternal diet on birth outcomes: a birth cohort study in Korea

Residential environmental exposures and other characteristics associated with detectable PAH-DNA adducts in peripheral mononuclear cells in a population-based sample of adult females

A Critical Evaluation of DNA Adducts as Biological Markers for Human Exposure to Polycyclic Aromatic Compounds

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