Ethnic Differences of Urinary Cadmium in Cigarette Smokers from the Multiethnic Cohort Study.
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ABSTRACT:
SUBMITTER: Cigan SS
PROVIDER: S-EPMC7967490 | biostudies-literature |
REPOSITORIES: biostudies-literature
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Project description:BackgroundIncidence rates of epithelial ovarian cancer (EOC) vary across racial/ethnic groups, yet little is known about the impact of hormone-related EOC risk factors in non-Whites.MethodsAmong 91,625 female Multiethnic Cohort Study participants, 155 incident EOC cases were diagnosed in Whites, 93 in African Americans, 57 in Native Hawaiians, 161 in Japanese Americans, and 141 in Latinas. We used Cox proportional hazards regression models to estimate hazard ratios (HR) and 95% confidence intervals (CI) for associations between race/ethnicity and EOC risk and between hormone-related factors and EOC risk across racial/ethnic groups.ResultsCompared with Whites, African Americans and Japanese Americans had a lower multivariable-adjusted EOC risk; Native Hawaiians had a suggestive higher risk. Parity and oral contraceptive (OC) use were inversely associated with EOC risk (P int race/ethnicity ≥ 0.43); associations were strongest among Japanese Americans (e.g., ≥4 vs. 0 children; HR = 0.45; CI, 0.26-0.79). Age at natural menopause and postmenopausal hormone (PMH) use were not associated with EOC risk in the overall population, but were positively associated with risk in Latinas (e.g., ≥5 years vs. never PMH use; HR = 2.13; CI, 1.30-3.49).ConclusionsWe observed strong associations with EOC risk for parity and OC use in Japanese Americans and PMH use and age at natural menopause in Latinas. However, differences in EOC risk among racial/ethnic groups were not fully explained by established hormone-related risk factors.ImpactOur study indicates there are racial/ethnic differences in EOC risk and risk factors, and could help improve prevention strategies for non-White women.
| S-EPMC7541726 | biostudies-literature
Project description:BackgroundWe previously found that African Americans and Native Hawaiians were at highest lung cancer risk compared with Japanese Americans and Latinos; whites were midway in risk. These differences were more evident at relatively low levels of smoking intensity, fewer than 20 cigarettes per day (CPD), than at higher intensity.MethodsWe apportioned lung cancer risk into three parts: age-specific background risk (among never smokers), an excess relative risk term for cumulative smoking, and modifiers of the smoking effect: race and years-quit smoking. We also explored the effect of replacing self-reports of CPD with a urinary biomarker-total nicotine equivalents-using data from a urinary biomarker substudy.ResultsTotal lung cancers increased from 1979 to 4993 compared to earlier analysis. Estimated excess relative risks for lung cancer due to smoking for 50 years at 10 CPD (25 pack-years) ranged from 21.9 (95% CI = 18.0 to 25.8) for Native Hawaiians to 8.0 (95% CI = 6.6 to 9.4) for Latinos over the five groups. The risk from smoking was higher for squamous cell carcinomas and small cell cancers than for adenocarcinomas. Racial differences consistent with earlier patterns were seen for overall cancer and for cancer subtypes. Adjusting for predicted total nicotine equivalents, Japanese Americans no longer exhibit a lower risk, and African Americans are no longer at higher risk, compared to whites. Striking risk differences between Native Hawaiians and Latinos persist.ConclusionsRacial differences in lung cancer risk persist in the Multiethnic Cohort study that are not easily explained by variations in self-reported or urinary biomarker-measured smoking intensities.
| S-EPMC6695313 | biostudies-literature
Project description:PurposeOlder age, African ancestry, and family history of prostate cancer are well-established risk factors for prostate cancer, and all are non-modifiable. Various lifestyle factors have been examined in relation to prostate cancer risk, including diet, obesity, and physical activity; however, none of them has been consistently related to risk. In the Multiethnic Cohort Study, we investigated whether lifestyle-related factors are associated with prostate cancer risk and whether such factors explain the racial/ethnic differences in risk.MethodsDuring a mean follow-up of 13.9 years, 7,115 incident cases were identified among 75,216 white, African-American, Native Hawaiian, Japanese American, and Latino men. Cox proportional hazards models were used to calculate relative risks (RRs) and 95 % confidence intervals (95 % CIs) for prostate cancer.ResultsAmong selected lifestyle-related factors including body mass index, height, education, physical activity, and intakes of alcohol, calcium, legumes, lycopene, and selenium, only smoking (RR for current (≥20 cigarettes/day) vs. never smoking = 0.72; 95 % CI 0.63-0.83) and history of diabetes (RR for yes vs. no = 0.78; 95 % CI 0.72-0.85) were significantly associated with prostate cancer risk. Compared to whites, the risk of incident prostate cancer was twofold higher in African-Americans and 16 % higher in Latinos. Additional adjustment for a history of PSA testing did not change the results.ConclusionsThe findings suggest that racial/ethnic differences in prostate cancer risk are not explained by the lifestyle factors examined and that underlying genetic factors may be involved.
| S-EPMC4567936 | biostudies-literature
Project description:There are racial/ethnic differences in the incidence of hormone receptor positive and negative breast cancer. To understand why these differences exist, we investigated associations between hormone-related factors and breast cancer risk by race/ethnicity in the Multiethnic Cohort (MEC) Study. Among 81 511 MEC participants (Native Hawaiian, Japanese American, Latina, African American and White women), 3806 estrogen receptor positive (ER+) and 828 ER- incident invasive breast cancers were diagnosed during a median of 21 years of follow-up. We used Cox proportional hazards regression models to calculate associations between race/ethnicity and breast cancer risk, and associations between hormone-related factors and breast cancer risk by race/ethnicity. Relative to White women, ER+ breast cancer risk was higher in Native Hawaiians and lower in Latinas and African Americans; ER- disease risk was higher in African Americans. We observed interaction with race/ethnicity in associations between oral contraceptive use (OC; Pint .03) and body mass index (BMI; Pint .05) with ER+ disease risk; ever versus never OC use increased risk only in Latinas and positive associations for obese versus lean BMI were strongest in Japanese Americans. For ER- disease risk, associations for OC use, particularly duration of use, were strongest for African Americans (Pint .04). Our study shows that associations of OC use and obesity with ER+ and ER- breast cancer risk differ by race/ethnicity, but established risk factors do not fully explain racial/ethnic differences in risk. Further studies are needed to identify factors to explain observed racial/ethnic differences in breast cancer incidence.
| S-EPMC8627491 | biostudies-literature
Project description:BackgroundEthnic disparities in metabolic disease risk may be the result of differences in circulating adipokines and inflammatory markers related to ethnic variations in obesity and body fat distribution.Subjects/methodsIn a cross-sectional design, we compared serum levels of leptin, adiponectin, C-reactive protein (CRP), interleukin-6 (IL-6) and tumor necrosis factor-α (TNF-α) in control subjects (321 men and 930 women) from two nested case-control studies conducted within the Multiethnic Cohort Study consisting of whites, Japanese Americans (JA), Latinos, African Americans (AA) and Native Hawaiians (NH). General linear models were applied to evaluate ethnic differences in log-transformed serum biomarker levels before and after adjusting for body mass index (BMI) at cohort entry.ResultsIn comparison to whites, significant ethnic differences were observed for all biomarkers except TNF-α. JA men and women had significantly lower leptin and CRP levels than whites, and JA women also had lower adiponectin levels. Leptin was significantly higher in AA women (P < 0.01), adiponectin was significantly lower in AA men and women (P = 0.02 and P < 0.001), and CRP and IL-6 were significantly higher in AA men and women. Lower adiponectin (P < 0.0001) and CRP (P = 0.03) levels were the only biomarkers in NH women that differed from whites; no statistically significant differences were seen for NH men and for Latino men and women. When adjusted for BMI at cohort entry, the differences between the lowest and the highest values across ethnic groups decreased for all biomarkers except adiponectin in men indicating that ethnic differences were partially due to weight status.ConclusionsThese findings demonstrate the ethnic variations in circulating adipokine and CRP levels before and after adjustment for BMI. Given the limitation of BMI as a general measure of obesity, further investigation with visceral and subcutaneous adiposity measures are warranted to elucidate ethnicity-related differences in adiposity in relation to disparities in obesity-related disease risk.
| S-EPMC4247246 | biostudies-literature
Project description:IntroductionSociodemographic differences in electronic cigarette use among cigarette smokers have not been previously characterized in the US adult population.MethodsWe analyzed longitudinal data from Waves 1 and 2 of the nationally representative Population Assessment of Tobacco and Health (PATH) study. Differences by income (based on federal poverty level (FPL)) and race/ethnicity in e-cigarette uptake at Wave 2 among cigarette smokers who were e-cigarette nonusers at Wave 1 were assessed using binomial and multinomial logistic regression. We differentiated e-cigarette users who quit cigarettes (exclusive users) from those who did not quit cigarettes (dual users). E-cigarette-related attitudes/beliefs were evaluated to understand potential contributions to sociodemographic differences in e-cigarette uptake and use patterns.ResultsAmong 6592 smokers who were e-cigarette nonusers at Wave 1, 13.5% began using e-cigarettes at Wave 2, of whom 91.3% were dual users. Compared with non-Hispanic Whites, non-Hispanic Black, and Hispanics were less likely to become exclusive e-cigarette users (OR [Blacks] = 0.27, 95% CI = 0.09 to 0.77; OR [Hispanics] = 0.26, 95% CI = 0.09 to 0.70). Low-income smokers were less likely than higher-income smokers to become exclusive e-cigarette users (OR [<100% FPL vs. ?200% FPL] = 0.48, 95% CI = 0.27 to 0.89). Black, Hispanic, and low-income smokers were more likely to believe e-cigarettes are more harmful than cigarettes and to have positive tobacco-related social norms.ConclusionsBlack, Hispanic, and low-income smokers were less likely than White and higher-income smokers to begin using e-cigarettes in the context of quitting cigarettes. Differences in e-cigarette uptake may be partly explained by perceived harm or social norms of e-cigarettes.ImplicationsResults of this study show that the exclusive use of e-cigarettes is more prevalent in higher-income and White smokers. Our data suggest that higher-income and White smokers may be more likely to use e-cigarettes as a means to quit combustible cigarettes compared with low-income and racial/ethnic minority smokers. These findings suggest that sociodemographic differences in e-cigarette uptake and use patterns may contribute to widening disparities in cigarette smoking.
| S-EPMC6751515 | biostudies-literature
Project description:BackgroundEpidemiologic studies suggest cadmium exposure is associated with cardiovascular disease risk, including heart failure. However, prior findings may be influenced by tobacco smoking, a dominant source of cadmium exposure and risk factor for heart failure. The present study leverages up to 20 years of follow-up in the Danish Diet, Cancer and Health cohort to examine the relationship between urinary cadmium and incident heart failure among people who never smoked.MethodsBetween 1993 and 1997, 19,394 never-smoking participants (ages 50-64 years) enrolled and provided a urine sample. From this sample, we randomly selected a subcohort of 600 men and 600 women and identified 958 incident heart failure cases occurring between baseline and 2015. Using a case-cohort approach, we estimated adjusted hazard ratios (aHR) for heart failure in Cox proportional hazards models with age as the time scale.ResultsParticipants had relatively low concentrations of urinary cadmium, as expected for never smokers (median = 0.20; 25th, 75th = 0.13, 0.32 μg cadmium/g creatinine). In adjusted models, we found that higher urinary cadmium was associated with a higher rate of incident heart failure overall (aHR = 1.1 per interquartile range difference [95% CI = 1.0, 1.2). In sex-stratified analyses, the association seemed restricted to men (aHR = 1.5 [95% CI = 1.2, 1.9]).ConclusionsIn this cohort of people who never smoked tobacco, environmental cadmium was positively associated with incident heart failure, especially among men.
| S-EPMC8810592 | biostudies-literature
Project description:BackgroundThe epidemiologic evidence from observational studies on breast cancer risk and phthalates, endocrine disrupting chemicals, has been inconsistent. In the only previous study based on pre-diagnostic urinary phthalates and risk of breast cancer, results were null in mostly white women.MethodsWe examined the association between pre-diagnostic urinary phthalates and breast cancer in a nested case-control study within the Multiethnic Cohort (MEC) study, presenting the first data from five major racial/ethnic groups in the USA. We measured 10 phthalate metabolites and phthalic acid, using a sensitive liquid chromatography mass spectrometry assay on 1032 women with breast cancer (48 African Americans, 77 Latinos, 155 Native Hawaiians, 478 Japanese Americans, and 274 Whites) and 1030 matched controls. Conditional logistic regression was used to examine risk with individual metabolites and ratios of primary (MEHP, mono-2-ethylhexyl-phthalate) to secondary (MEHHP, mono(2-ethyl-5-hydroxyhexyl); MEOHP, mono(2-ethyl-5-oxohexy)) metabolites of di-2-ethylhexyl phthalate (DEHP), a widely used plasticizer. In addition, we investigated risk associations with high (∑HMWP) and low molecular weight (∑LMWP) phthalates, as well as total phthalates which included high and low molecular weight phthalates with phthalic acid (∑LMHMPA) or without phthalic acid in molar ratios (∑LMHMmolar) and adjusted for creatinine and potential confounders.ResultsAmong all women, breast cancer risk was higher for those in tertile 2 and tertile 3 of primary to secondary metabolites of DEHP (MEHP/(MEHHP + MEOHP)) in comparison to those in tertile 1; the respective odds ratios were 1.32 (95% CI 1.04-1.68) and 1.26 (95% CI 0.96-1.66) (Ptrend = 0.05). Risk among Native Hawaiian women increased with exposures to eight of ten individual phthalates and total phthalates (∑LMHMPA ORT3 vs T1 = 2.66, 95% CI 1.39-5.12, Ptrend = 0.001). In analysis by hormone receptor (HR) status, exposure above the median of ∑LMWP was associated with an increased risk of HR-positive breast cancer (OR = 1.30, 95% CI 1.05-1.60) while above the median exposure to phthalic acid was associated with an increased risk of HR-negative breast cancer (ORabove vs below median = 1.59, 95% CI 1.01-2.48).ConclusionsFurther investigations of suggestive associations of elevated breast cancer risk with higher ratios of primary to secondary metabolites of DEHP, and differences in risk patterns by race/ethnicity and HR status are warranted.
| S-EPMC8025373 | biostudies-literature
Project description:While smoking is the primary cause of lung cancer, only 11-24% of smokers develop the malignancy over their lifetime. The primary addictive agent in tobacco smoke is nicotine and variation in nicotine metabolism may influence the smoking levels of an individual. Therefore, inter-individual variation in lung cancer risk among smokers may be due in part to differences in the activity of enzymes involved in nicotine metabolism. In most smokers, cytochrome P450 2A6 (CYP2A6)-catalyzed C-oxidation accounts for >75% of nicotine metabolism, and the activity of this enzyme has been shown to correlate with the amount of nicotine and carcinogens drawn from cigarettes. We prospectively evaluated the association of urinary biomarkers of nicotine uptake (total nicotine equivalents [TNE]) and CYP2A6 activity (ratio of urinary total trans-3'-hydroxycotinine to cotinine) with lung cancer risk among 2,309 Multiethnic Cohort Study participants who were current smokers at time of urine collection; 92 cases were diagnosed during a mean follow-up of 9.5 years. We found that higher CYP2A6 activity and TNE was associated with increased lung cancer risk after adjusting for age, sex, race/ethnicity, body mass index, smoking duration, and urinary creatinine (p's = 0.002). The association for CYP2A6 activity remained even after adjusting for self-reported cigarettes per day (CPD) (Hazard Ratio [HR] per unit increase in log-CYP2A6 activity = 1.52; p = 0.005) and after adjusting for TNE (HR = 1.46; p = 0.01). In contrast, the association between TNE and lung cancer risk was of borderline statistical significance when adjusted for CPD (HR = 1.53; p = 0.06) and not statistically significant when further adjusted for CYP2A6 activity (HR = 1.30; p = 0.22). These findings suggest that CYP2A6 activity provides information on lung cancer risk that is not captured by smoking history or a (short-term) biomarker of dose. CYP2A6 activity should be further studied as a risk biomarker for smoking-related lung cancer.
| S-EPMC5444837 | biostudies-literature