Sources of Tobacco Smoke Exposure and Their Associations With Serum Cotinine Levels Among US Children and Adolescents.

INTRODUCTION: We assessed tobacco smoke exposure (TSE) levels based on private and public locations of TSE according to race and ethnicity among US school-aged children ages 6-11 years and adolescents ages 12-17 years. AIMS AND METHODS: Data were from 5296 children and adolescents who participated in the National Health and Nutrition Examination Survey (NHANES) 2013-2018. Racial and ethnic groups were non-Hispanic white, black, other or multiracial, and Hispanic. NHANES assessed serum cotinine and the following TSE locations: homes and whether smokers did not smoke indoors (home thirdhand smoke [THS] exposure proxy) or smoked indoors (secondhand [SHS] and THS exposure proxy), cars, in other homes, restaurants, or any other indoor area. We used stratified weighted linear regression models by racial and ethnic groups and assessed the variance in cotinine levels explained by each location within each age group. RESULTS: Among 6-11-year-olds, exposure to home THS only and home SHS + THS predicted higher log-cotinine among all racial and ethnic groups. Non-Hispanic white children exposed to car TSE had higher log-cotinine (ß = 1.64, 95% confidence interval [CI] = 0.91% to 2.37%) compared to those unexposed. Non-Hispanic other/multiracial children exposed to restaurant TSE had higher log-cotinine (ß = 1.13, 95% CI = 0.23% to 2.03%) compared to those unexposed. Among 12-17-year-olds, home SHS + THS exposure predicted higher log-cotinine among all racial and ethnic groups, except for non-Hispanic black adolescents. Car TSE predicted higher log-cotinine among all racial and ethnic groups. Non-Hispanic black adolescents with TSE in another indoor area had higher log-cotinine (ß = 2.84, 95% CI = 0.85% to 4.83%) compared to those unexposed. CONCLUSIONS: TSE location was uniquely associated with cotinine levels by race and ethnicity. Smoke-free home and car legislation are needed to reduce TSE among children and adolescents of all racial and ethnic backgrounds. IMPLICATIONS: Racial and ethnic disparities in TSE trends have remained stable among US children and adolescents over time. This study's results indicate that TSE locations differentially contribute to biochemically measured TSE within racial and ethnic groups. Home TSE significantly contributed to cotinine levels among school-aged children 6-11 years old, and car TSE significantly contributed to cotinine levels among adolescents 12-17 years old. Racial and ethnic differences in locations of TSE were observed among each age group. Study findings provide unique insight into TSE sources, and indicate that home and car smoke-free legislation have great potential to reduce TSE among youth of all racial and ethnic backgrounds.

Multilevel Intervention for Low-Income Maternal Smokers in the Special Supplemental Nutrition Program for Women, Infants, and Children (WIC).

Objectives. To test the efficacy of Babies Living Safe and Smokefree (BLiSS), a multilevel intervention initiated in a citywide safety net health system to improve low-income maternal smokers' abstinence and reduce child tobacco smoke exposure. Methods. This randomized controlled trial in Philadelphia, Pennsylvania (2015-2020), recruited low-income maternal smokers who received a brief smoking intervention (Ask, Advise, Refer [AAR]) from nutrition professionals in the Special Supplemental Nutrition Program for Women, Infants, and Children before randomization to (1) a multilevel intervention (AAR + multimodal behavioral intervention [MBI]; n = 199) or (2) an attention control intervention (AAR + control; n = 197). Results. AAR + MBI mothers had significantly higher 12-month bioverified abstinence rates than did AAR + control mothers (odds ratio [OR] = 9.55; 95% confidence interval [CI] = 1.54, 59.30; P = .015). There were significant effects of time (b = -0.15; SE = 0.04; P < .001) and condition by time (b = -0.19; SE = 0.06; P < .001) on reported child exposure favoring AAR + MBI, but no group difference in child cotinine. Presence of other residential smokers was related to higher exposure. Higher baseline nicotine dependence was related to higher child exposure and lower abstinence likelihood at follow-up. Conclusions. The multilevel BLiSS intervention was acceptable and efficacious in a population that experiences elevated challenges with cessation. Public Health Implications. BLiSS is a translatable intervention model that can successfully improve efforts to address the persistent tobacco-related burdens in low-income communities. Trial Registration. Clinical Trials.gov identifier: NCT02602288. (Am J Public Health. 2022;112(3):472-481. https://doi.org/10.2105/AJPH.2021.306601).

Racial disparities in intensity of smoke exposure and nicotine intake among low-dependence smokers.

BACKGROUND: Compared to white smokers, Black smokers are at disproportionately higher risk for smoking-related disease, despite consuming fewer cigarettes per day (CPD). To examine racial disparities in biobehavioral influences on smoking and disease risk, we analyzed the relationship between self-reported tobacco dependence and intensity of tobacco smoke exposure per cigarette, on the one hand, and intensity of nicotine intake per cigarette, on the other. METHODS: In 270 Black and 516 white smokers, smoke exposure was measured by expired carbon monoxide (CO), and nicotine intake was measured by plasma cotinine (COT) and cotinine+3'-hydroxycotinine ([COT + 3HC]). Using linear regression analyses, we analyzed how the Fagerström Test for Cigarette Dependence (FTCD) predicted intensity of smoke exposure per cigarette (CO/CPD) and intensity of nicotine intake per cigarette (COT/CPD; [COT + 3HC]/CPD), and how race moderated these relations. RESULTS: Overall, Black smokers consumed fewer CPD than white smokers and had higher levels of CO/CPD, COT/CPD, and [COT + 3HC]/CPD. These elevations were most pronounced at lower levels of dependence: amongst Black smokers, FTCD negatively predicted intensity of smoke exposure as measured by CO/CPD (B = -0.12, 95% CI = -0.18, -0.05, p = 0.0003) and intensity of nicotine intake as measured by [COT + 3HC]/CPD (B = -1.31, 95% CI = -2.15, -0.46, p = 0.002). CONCLUSIONS: Low-dependence Black smokers had higher intensities of both smoke exposure and nicotine intake per cigarette compared to similarly dependent white smokers, suggesting that measures of dependence, exposure, and intake underestimate incremental risk of each cigarette to Black smokers.

Linkage of Maternal Caregiver Smoking Behaviors on Environmental and Clinical Outcomes of Children with Asthma: A Post-Hoc Analysis of a Financial Incentive Trial Targeting Reduction in Pediatric Tobacco Smoke Exposures.

(1) Background: Monthly variability in smoking behaviors in caregivers of pediatric asthmatics yields questions of how much and when does smoking reduction result in improved environmental and clinical outcomes. (2) Methods: Post hoc analysis of data from a 6 month pilot randomized-control trial occurring from May 2017 to May 2018 in Baltimore City (MD, USA). The initial trial's primary intervention explored the utility of financial incentives in modifying caregiver smoking behaviors. Post hoc analyses examined all dyads independent of the initial trial's randomization status. All caregivers received pediatric tobacco smoke harm reduction education, in addition to monthly encouragement to access the state tobacco quitline for individual phone-based counseling and nicotine replacement therapy. Maternal caregivers who were active cigarette smokers and their linked asthmatic child (aged 2-12 years) were grouped into two classifications ("high" versus "low") based on the child and caregiver's cotinine levels. A "low" cotinine level was designated by at least a 25% reduction in cotinine levels during 3 months of the trial period; achieving ≤2 months of low cotinine levels defaulted to the "high" category. Twenty-seven dyads (caregivers and children) (total n = 54) were assigned to the "high" category, and eighteen dyads (caregivers and children) (total n = 36) were allocated to the "low" category. The primary outcome measure was the correlation of caregiver cotinine levels with pediatric cotinine values. Secondary outcomes included asthma control, in addition to caregiver anxiety and depression. (3) Results: Caregivers with 3 months of ≥25% decrease in cotinine levels had a significantly greater mean change in child cotinine levels (p = 0.018). "Low" caregiver cotinine levels did not significantly improve pediatric asthma control (OR 2.12 (95% CI: 0.62-7.25)). Caregiver anxiety and depression outcomes, measured by Patient Health Questionnaire (PHQ)-4 scores, was not significantly different based on cotinine categorization (p = 0.079); (4) Conclusion: Reduced pediatric cotinine levels were seen in caregivers who reduced their smoking for at least 3 months, but clinical outcome measures remained unchanged.

The Use of the Nicotine Metabolite Ratio as a Biomarker to Personalize Smoking Cessation Treatment: Current Evidence and Future Directions.

The nicotine metabolite ratio (NMR), a genetically informed biomarker of rate of nicotine metabolism, has been validated as a tool to select the optimal treatment for individual smokers, thereby improving treatment outcomes. This review summarizes the evidence supporting the development of the NMR as a biomarker of individual differences in nicotine metabolism, the relationship between the NMR and smoking behavior, the clinical utility of using the NMR to personalize treatments for smoking cessation, and the potential mechanisms that underlie the relationship between NMR and smoking cessation. We conclude with a call for additional research necessary to determine the ultimate benefits of using the NMR to personalize treatments for smoking cessation. These future directions include measurement and other methodologic considerations, disseminating this approach to at-risk subpopulations, expanding the NMR to evaluate its efficacy in predicting treatment responses to e-cigarettes and other noncigarette forms of nicotine, and implementation science including cost-effectiveness analyses.See all articles in this Special Collection Honoring Paul F. Engstrom, MD, Champion of Cancer Prevention.

Use of Potentially Reduced Exposure Tobacco Products Among American Indian Smokeless Tobacco Users: Associations With Cessation Behaviors and Cotinine Levels.

OBJECTIVES: American Indian/Alaska Native (AI/AN) adults use smokeless tobacco products (eg, chewing and dip tobacco) more often than other racial/ethnic groups do. Although US adults increasingly use potentially reduced exposure tobacco products (PREPs), such as electronic cigarettes and snus, no studies have examined the use of PREPs among AI/AN smokeless tobacco users. We examined associations between current PREPs use and smokeless tobacco-related measures, including cessation attempts and cotinine levels, in a sample of American Indian adults who currently use smokeless tobacco. METHODS: We collected survey and tobacco biomarker data from 299 adult American Indian smokeless tobacco users at Cherokee Nation health care facilities and events in 2016 and 2017. We used multivariable analyses to determine associations between current PREPs use and smokeless tobacco-related characteristics. RESULTS: Current PREPs users were younger, less likely to be married or living with a partner, less likely to report a chronic medical condition, and more likely to report other tobacco use than PREPs nonusers. Among participants with annual household incomes ≤$30 000, current PREPs users were less likely than PREPs nonusers to report a definite desire to quit smokeless tobacco (P = .02). PREPs use was not associated with planning to quit smokeless tobacco, past 12-month smokeless tobacco quit attempts, amount of smokeless tobacco used per week, cotinine levels, or scores on the Fagerström Test for Nicotine Dependence-Smokeless Tobacco. CONCLUSIONS: Our study suggests that American Indian smokeless tobacco users may not be using PREPs as a smokeless tobacco cessation aid. Future studies should take this finding into consideration when evaluating the role of PREPs use in smokeless tobacco cessation and in total tobacco cessation in this population.

Environmental Tobacco Smoke Exposure in Relation to Family Characteristics, Stressors and Chemical Co-Exposures in California Girls.

Childhood environmental tobacco smoke (ETS) exposure is a risk factor for adverse health outcomes and may disproportionately burden lower socioeconomic status groups, exacerbating health disparities. We explored associations of demographic factors, stressful life events, and chemical co-exposures, with cotinine levels, among girls in the CYGNET Study. Data were collected from families of girls aged 6-8 years old in Northern California, through clinic exams, questionnaires and biospecimens (n = 421). Linear regression and factor analysis were conducted to explore predictors of urinary cotinine and co-exposure body burdens, respectively. In unadjusted models, geometric mean cotinine concentrations were higher among Black (0.59 ug/g creatinine) than non-Hispanic white (0.27), Asian (0.32), or Hispanic (0.34) participants. Following adjustment, living in a rented home, lower primary caregiver education, and lack of two biologic parents in the home were associated with higher cotinine concentrations. Girls who experienced parental separation or unemployment in the family had higher unadjusted cotinine concentrations. Higher cotinine was also associated with higher polybrominated diphenyl ether and metals concentrations. Our findings have environmental justice implications as Black and socio-economically disadvantaged young girls experienced higher ETS exposure, also associated with higher exposure to other chemicals. Efforts to reduce ETS and co-exposures should account for other disparity-related factors.

Exposure to Secondhand Smoke Among Nonsmokers - United States, 1988-2014.

Exposure to secondhand smoke from burning tobacco products can cause sudden infant death syndrome, respiratory infections, ear infections, and asthma attacks in infants and children, and coronary heart disease, stroke, and lung cancer in adult nonsmokers (1). There is no risk-free level of secondhand smoke exposure (2). CDC analyzed questionnaire and laboratory data from the National Health and Nutrition Examination Survey (NHANES) to assess patterns of secondhand smoke exposure among U.S. nonsmokers. The prevalence of secondhand smoke exposure among U.S. nonsmokers declined substantially during 1988-2014, from 87.5% to 25.2%. However, no change in exposure occurred between 2011-2012 and 2013-2014, and an estimated one in four nonsmokers, or approximately 58 million persons, were still exposed to secondhand smoke during 2013-2014. Moreover, marked disparities persisted across population groups. Exposure prevalence was highest among nonsmokers aged 3-11 years (37.9%), non-Hispanic blacks (50.3%), and those who were living in poverty (47.9%), in rental housing (38.6%), or with someone who smoked inside the home (73.0%), or among persons who had less than a high school education (30.7%). Comprehensive smoke-free laws and policies for workplaces and public places and smoke-free rules for homes and vehicles can further reduce secondhand smoke exposure among all nonsmokers.

Exposure to tobacco smoke and validation of smoking status during pregnancy in the MIREC study.

Given that prenatal exposure to tobacco smoke can lead to increased risks of adverse health effects, having valid measures of exposure is important. In a Canadian cohort (n = 2000), maternal and infant biospecimens were analysed for cotinine. Sensitivity and specificity of self-reported active smoking status were estimated. Regression modelling was used to identify potential predictors of maternal and infant plasma cotinine in non-smoking women. During the first trimester, 60.6% of the women reported never smoking, 27.3% were former smokers, 6.1% had quit when they found out they were pregnant, 5.8% were smokers and 42% of the non-smokers reported exposure to secondhand smoke (SHS). Low detection of tobacco biomarkers in meconium limited its ability to identify exposure to SHS. The sensitivity and specificity for self-reported smoking during the 1st trimester were 85.37 and 99.45%, respectively. The lowest sensitivity was found in participants with the highest level of education and income, oldest women and those born outside Canada. Non-smoking women living in an apartment had 1.7 times higher odds of detectable plasma cotinine than those living in a single home after adjusting for other variables. Our results suggest that while self-reports are fairly accurate, they may be less so in populations with higher socio-economic status. This investigation underscores the need to consider the participant socio-economic characteristics and dwelling type when using questionnaires to estimate active and passive tobacco exposure.

Heterogeneity in Smokers' Responses to Tobacco Control Policies.

This paper uses unconditional quantile regression to estimate whether smokers' responses to tobacco control policies change across the distribution of smoking levels. I measure smoking behavior with the number of cigarettes smoked per day and also with serum cotinine levels, a continuous biomarker of nicotine exposure, using individual-level repeated cross-section data from the National Health and Nutrition Examination Surveys. I find that the cigarette taxes lead to reductions in both the number of cigarettes smoked per day and in smokers' cotinine levels. These reductions are most pronounced in the middle quantiles of both distributions in terms of marginal effects, but most pronounced in the lower quantiles in terms of tax elasticities. I do not find that higher cigarette taxes lead to statistically significant changes in the amount of nicotine smokers ingest from each cigarette. Copyright © 2015 John Wiley & Sons, Ltd.

Income Inequality and US Children's Secondhand Smoke Exposure: Distinct Associations by Race-Ethnicity.

INTRODUCTION: Prior studies have found considerable racial and ethnic disparities in secondhand smoke (SHS) exposure. Although a number of individual-level determinants of this disparity have been identified, contextual determinants of racial and ethnic disparities in SHS exposure remain unexamined. The objective of this study was to examine disparities in serum cotinine in relation to area-level income inequality among 14 649 children from the National Health and Nutrition Examination Survey. METHODS: We fit log-normal regression models to examine disparities in serum cotinine in relation to Metropolitan Statistical Areas level income inequality among 14 649 nonsmoking children aged 3-15 from the National Health and Nutrition Examination Survey (1999-2012). RESULT: Non-Hispanic black children had significantly lower serum cotinine than non-Hispanic white children (-0.26; 95% CI: -0.38, -0.15) in low income inequality areas, but this difference was attenuated in areas with high income inequality (0.01; 95% CI: -0.16, 0.18). Serum cotinine declined for non-Hispanic white and Mexican American children with increasing income inequality. Serum cotinine did not change as a function of the level of income inequality among non-Hispanic black children. CONCLUSIONS: We have found evidence of differential associations between SHS exposure and income inequality by race and ethnicity. Further examination of environments which engender SHS exposure among children across various racial/ethnic subgroups can foster a better understanding of how area-level income inequality relates to health outcomes such as levels of SHS exposure and how those associations differ by race/ethnicity. IMPLICATIONS: In the United States, the association between children's risk of SHS exposure and income inequality is modified by race/ethnicity in a manner that is inconsistent with theories of income inequality. In overall analysis this association appears to be as predicted by theory. However, race-specific analyses reveal that higher levels of income inequality are associated with lower levels of SHS exposure among white children, while levels of SHS exposure among non-Hispanic black children are largely invariant to area-level income inequality. Future examination of the link between income inequality and smoking-related health outcomes should consider differential associations across racial and ethnic subpopulations.

Pitfalls in the assessment of smoking status detected in a cohort of South African RA patients.

This study was conceived in an attempt to explain the unexpectedly high frequency of elevated levels of serum cotinine measured retrospectively in a cohort of predominantly black South African females with rheumatoid arthritis (RA), findings that were inconsistent with the smoking histories derived from health questionnaires. The discrepant findings suggested either a greater tendency towards underreporting of smoking status in the study cohort, or possible confounding effects of the use of smokeless tobacco products. In addition to the cohort of RA patients (n = 138, of whom 115 (83 %) were female), blood samples were also taken from a second cohort consisting of 29 declared smokers, 18 (62 %) of whom where females, 29 smokeless tobacco (SLT) users (all female), and 22 non-users of any tobacco products, 18 (82 %) of whom were females. Serum cotinine levels were determined using an ELISA procedure. Cotinine levels of >10.0 ng/ml were detected in serum specimens from 43 (31 %), RA patients of whom 35 (81 %) were female, with a median value of 50.1 ng/ml and interquartile range (iqr) of 68.6. Only 18 of the 35 females indicated that they smoked. The groups of declared smokers and SLT users had equivalent median serum cotinine levels of 88.0 ng/ml (iqr = 10.8 ng/ml) and 87.0 ng/ml (iqr = 15.6 ng/ml), respectively, while cotinine was undetectable in specimens from non-tobacco product users (<0.2 ng/ml). Users of SLT products in South Africa are predominantly female and have serum cotinine levels which are comparable with those of current smokers, raising concerns about the validity of measurement of cotinine as the sole objective marker of smoking status in populations with high usage of SLTs. This situation can be rectified by ensuring that usage of SLT products is accurately recorded in health questionnaires, while inclusion of measurement of one or more additional, objective biomarkers of smoking in combination with cotinine may enable reliable distinction between smoking and usage of SLTs which, given the associated risks, is a strategy of particular relevance in RA.

Toxicological assessment of a prototype e-cigaret device and three flavor formulations: a 90-day inhalation study in rats.

A prototype electronic cigaret device and three formulations were evaluated in a 90-day rat inhalation study followed by a 42-day recovery period. Animals were randomly assigned to groups for exposure to low-, mid- and high-dose levels of aerosols composed of vehicle (glycerin and propylene glycol mixture); vehicle and 2.0% nicotine; or vehicle, 2.0% nicotine and flavor mixture. Daily targeted aerosol total particulate matter (TPM) doses of 3.2, 9.6 and 32.0 mg/kg/day were achieved by exposure to 1 mg/L aerosol for 16, 48 and 160 min, respectively. Pre-study evaluations included indirect ophthalmoscopy, virology and bacteriological screening. Body weights, clinical observations and food consumption were monitored weekly. Plasma nicotine and cotinine and carboxyhemoglobin levels were measured at days 28 and 90. After days 28, 56 and 90, lung function measurements were obtained. Biological endpoints after 90-day exposure and 42-day recovery period included clinical pathology, urinalysis, bronchoalveolar fluid (BALF) analysis, necropsy and histopathology. Treatment-related effects following 90 days of exposure included changes in body weight, food consumption and respiratory rate. Dose-related decreases in thymus and spleen weights, and increased BALF lactate dehydrogenase, total protein, alveolar macrophages, neutrophils and lung weights were observed. Histopathology evaluations revealed sporadic increases in nasal section 1-4 epithelial hyperplasia and vacuolization. Following the recovery period, effects in the nose and BALF were persistent while other effects were resolved. The no observed effect level based upon body weight decreases is considered to be the mid-dose level for each formulation, equivalent to a daily TPM exposure dose of approximately 9.6 mg/kg/day.

Trends in exposure to second hand smoke at home among children and nonsmoker adolescents.

Data from National Health and Nutrition Examination Survey (NHANES) for the years 1999-2012 were used to evaluate trends in exposure to second hand smoke (SHS) at home among children aged 3-11 years and nonsmoker adolescents aged 12-19 years. A total of 12,815 children and 10,269 adolescents were included in the analyses. Serum cotinine was used as a biomarker for exposure to SHS at home. Regression models with log10 transformed values of serum cotinine as dependent variables and age, race/ethnicity, NHANES survey year, and family poverty income ratio as a surrogate measure of socioeconomic status were used in models for those with and without exposure to SHS at home. In addition, for those with exposure to SHS at home, number of smokers smoking inside home and number of cigarettes smoked at home every day were also used as independent variables. There was a biennial increase of 1.05 ng/L in adjusted serum cotinine levels for children with exposure to SHS at home over the period of 1999-2012. Serum cotinine levels among nonsmoker adolescents with exposure to SHS at home did not change over time. When there was no exposure to SHS at home, there was a statistically significant downward trend for serum cotinine levels for both children and nonsmoker adolescents. Serum cotinine levels attributable to SHS exposure increased with age among nonsmoker adolescents (p≤0.02) but decreased with age among children (p<0.01). For a unit decrease in family poverty income ratio, SHS exposure as measured by serum cotinine levels (Table 6) increased by 1.18 ng/L among children and by 1.30 ng/L among nonsmoker adolescents. In general, observed serum cotinine levels associated with SHS exposure at home were higher for children than they were for nonsmoker adolescents.

Associations Between Genetic Ancestries and Nicotine Metabolism Biomarkers in the Multiethnic Cohort Study.

Differences in internal dose of nicotine and tobacco-derived carcinogens among ethnic/racial groups have been observed. In this study, we explicitly examined the relationships between genetic ancestries (genome-wide average) and 19 tobacco-derived biomarkers in smokers from 3 admixed groups in the Multiethnic Cohort Study (1993-present), namely, African ancestry in African Americans (n = 362), Amerindian ancestry in Latinos (n = 437), and Asian and Native Hawaiian ancestries in Native Hawaiians (n = 300). After multiple comparison adjustment, both African and Asian ancestries were significantly related to a greater level of free cotinine; African ancestry was also significantly related to lower cotinine glucuronidation (P's < 0.00156). The predicted decrease in cotinine glucuronidation was 8.6% (P = 4.5 × 10(-6)) per a 20% increase in African ancestry. Follow-up admixture mapping revealed that African ancestry in a 12-Mb region on chromosome 4q was related to lower cotinine glucuronidation (P's < 2.7 × 10(-7), smallest P = 1.5 × 10(-9)), although this is the same region reported in our previous genome-wide association study. Our results implicate a genetic ancestral component in the observed ethnic/racial variation in nicotine metabolism. Further studies are needed to identify the underlying genetic variation that could potentially be ethnic/racial specific.

The economic burden of exposure to secondhand smoke for child and adult never smokers residing in U.S. public housing.

OBJECTIVE: The World Health Organization (WHO) reports that nonsmokers experience disease and death due to secondhand smoke (SHS) exposure in the home. We estimated the total excess burden and costs to society due to SHS exposure in U.S. public housing. METHODS: We quantified the public health burden for outcomes causally related to SHS exposure for nationally representative never-smoking residents in U.S. public housing using (1) WHO-recommended health outcomes and methodology, (2) publicly available and other large databases, and (3) published estimates of morbidity and mortality rates. We used published estimates of direct medical and nonmedical care costs and the value of productivity losses to estimate SHS-related societal costs for disease and death. We estimated the public health and economic burden for two serum cotinine limits of detection (LODs): 0.05 nanograms per milliliter (ng/mL) and 0.015 ng/mL. RESULTS: In 2011, an estimated 37,791 never-smoking child and adult U.S. public housing residents experienced illness and death due to SHS exposure at home based on an LOD=0.05 ng/mL (50,967 residents at LOD=0.015 ng/mL). Costs incurred by society for these illnesses and deaths totaled $183 million (LOD=0.05 ng/mL) and $267 million (LOD=0.015 ng/mL) annually. Of the total costs, direct costs (medical and nonmedical) accounted for $128 million and $176 million for LOD=0.05 ng/mL and LOD=0.015 ng/mL, respectively. Medical care accounted for the majority of direct costs-$110 million at LOD=0.05 ng/mL and $153 million at LOD=0.015 ng/mL. Adverse respiratory health outcomes accounted for approximately one-half (56% at LOD=0.05 ng/mL and 52% at LOD=0.015 ng/mL) of total societal costs. CONCLUSION: Implementing smoke-free policies in all U.S. public housing could save lives and decrease SHS-related morbidity and mortality in never-smoking residents, resulting in annual societal savings of $183 million at LOD=0.05 ng/mL and $267 million at LOD=0.015 ng/mL.

Assessment of Cotinine Reveals a Dose-Dependent Effect of Smoking Exposure on Long-term Outcomes After Renal Transplantation.

BACKGROUND: Smoking is a risk factor for poor late outcomes in renal transplant recipients (RTR). Smoking exposure can be assessed by self-report and cotinine measurements. We investigated whether use of cotinine as a biomarker for smoking exposure can serve as an alternative for self-report and to compare associations of smoking exposure by self-report and cotinine with outcomes in RTR and assess dose dependency. METHODS: Renal transplant recipients were classified as never, former, light (≤10 cigarettes/day), and heavy smokers (>10 cigarettes/day) according to self-report and analogous categories for urine and plasma cotinine. First, we assessed agreement of self-reported smoking exposure with smoking exposure according urine and plasma cotinine. Second, we compared the associations with graft failure and mortality. RESULTS: Of 603 RTR (age 51.5 ± 12.1 years, 55% men), 36.0% RTR were never, 42.3% former, 10.6% light, and 11.1% heavy smokers according to self-report. The majority (98.6%) of never smokers had nondetectable cotinine. However, 14 and 13 RTR reporting no active smoking had respective urine or plasma cotinine consistent with active smoking. Cotinine-based measurements were dose-dependently associated with mortality and graft failure. CONCLUSIONS: Plasma and urine cotinine can serve as an alternative to self-report and were dose-dependently associated with poor late outcomes in RTR.

Vital signs: disparities in nonsmokers' exposure to secondhand smoke--United States, 1999-2012.

Exposure to secondhand smoke (SHS) from burning tobacco products causes sudden infant death syndrome (SIDS), respiratory infections, ear infections, and asthma attacks in infants and children, and coronary heart disease, stroke, and lung cancer in adult nonsmokers. No risk-free level of SHS exposure exists. SHS exposure causes more than 41,000 deaths among nonsmoking adults and 400 deaths in infants each year, and approximately $5.6 billion annually in lost productivity. Although population exposure to SHS has declined over the past 2 decades, many nonsmokers remain exposed to SHS in workplaces, public places, homes, and vehicles.

Plasma micronutrient levels and telomere length in children.

OBJECTIVE: Telomeres are long hexamer (TTAGGG) repeats at the ends of chromosomes, and contribute to maintenance of chromosomal stability. Telomere shortening has been linked to cancers and other chronic diseases in adults, although evidence for causal associations is limited. The aim of this study was to determine whether nutritional factors are associated with telomere length (TL) in children. METHODS: We conducted a cross-sectional study of nutritional factors and TL in 437 children between 2009 and 2011. Healthy children ages 3, 6, and 9 y provided blood samples, and their parents completed a food frequency questionnaire and a telephone interview about relevant environmental exposures. TL and blood micronutrient levels were measured, and genotyping at 10 loci was undertaken. Associations between the micronutrients and other variables were assessed using linear regression. RESULTS: No significant main or interactive effects of age or sex were seen. After adjustment for age, sex, parental education, and month of blood collection, TL was inversely associated with plasma zinc, and shorter in children with the homozygous mutant genotype of the RFC G80A (rs1051266) polymorphism. CONCLUSIONS: To the best of our knowledge, this is the first investigation of the association between telomere length and micronutrients in healthy children. The reason for the inverse relationship of TL with zinc is unknown but could be the result of an increase in telomere sequence deletions caused by labile zinc induction of oxidative stress. These findings should be corroborated in other studies before nutritional recommendations might be considered.

Population-based comparison of biomarker concentrations for chemicals of concern among Latino-American and non-Hispanic white children.

Differences in cultural and economic status may place ethnic subgroups of children at higher risk for exposure, leading to heightened health risks, and health inequities. Although Latino-Americans represent 22% of all children in the United States, few studies have explored within-group differences in their exposure to toxicants. Using socio-demographic and biomarker data from the National Health and Nutrition Examination Survey from 1999 to 2008, we characterized determinants of health and estimated geometric means of environmental contaminant biomarkers (blood concentrations of lead and mercury, serum concentrations of dichlorodiphenyldichloroethylene [p,p'-DDE] and cotinine, and urinary metabolites of organophosphate [OP] pesticides and polycyclic aromatic hydrocarbons [PAHs]) among 4,257 Mexican American (MA), 677 Other Latino-American (OL), and 3,370 Non-Hispanic White (NHW) children. MAs had the lowest levels of health insurance coverage and regular access to health care, and largest household size compared to NHWs and OLs. MAs had higher levels of p,p'-DDE, lead, and cadmium while OLs had higher estimates of mercury relative to other groups. MAs had higher urinary metabolite concentrations of 2-hydroxynaphthalene; otherwise MAs and OLs had lower concentrations of PAHs. NHWs had higher levels of cotinine and dimethylthiophosphate. For other OP metabolites, differences among groups were less clear. Lead and p,p'-DDE exposure differences likely reflect later and less regulatory control of these chemicals in Latin America. Additionally, poor quality housing with lead paint is more common in economically disadvantaged subpopulations. Dietary habits are possible sources of differential cadmium, mercury, and organophosphate exposure. Cotinine exposure differences by income and U.S.- vs. foreign-born may represent increased acculturation. These results, coupled with additional research on exposure sources may contribute to refinement of environmental health promotion programs for the fast-growing Latino-American population.