Active Tobacco Smoke Exposure Research Articles

Atopic dermatitis and tobacco smoke exposure during childhood and adolescence

Tobacco smoke may affect atopic dermatitis (AD) because of its known effects on humoral and cellular immunity, but prior studies lack data on disease severity and biomarkers over time. We investigated the association between passive and active tobacco smoke exposure (TSE) during childhood and adolescence and the activity and severity of AD. A birth cohort of 10,521 individuals was followed through adolescence as part of the Avon Longitudinal Study of Parents and Children. We used mixed-effect models to determine the risk of AD (based on repeated assessments) with passive smoke exposure during childhood, active TSE during adolescence, and using a serum biomarker of tobacco exposure (cotinine) at 3 time points. After adjusting for confounding factors, there was no evidence of a relationship between passive TSE and concurrent AD activity in childhood (adjusted odds ratio, 0.95; 95% confidence interval, 0.83, 1.07) or of an increased risk between active smoking and AD activity in adolescence (adjusted odds ratio, 0.57; 95% confidence interval, 0.44, 0.75). Secondary analyses demonstrated no dose-response relationship and no increased severity of AD with passive or active TSE. Furthermore, we found no increased risk of AD with a cumulative measure of passive TSE across childhood (adjusted relative risk ratio, 0.98; 95% confidence interval, 0.96, 1.00). Neither active nor passive TSE was associated with AD during childhood and adolescence.

Associations of active and passive tobacco exposure with elevated blood pressure in Korean adolescents.

To test the hypothesis that tobacco exposure is associated with elevated blood pressure (EBP) in Korean adolescents, and that the association is dose dependent. This cross-sectional study used data from the 2011-2020 Korea National Health and Nutrition Survey (KNHANES). Subjects were eligible if they were 13-18 years at the time of participation in KNHANES. Tobacco exposure was defined by urine cotinine level. The main outcomes were EBP and hypertension. Statistical analyses were conducted using SAS version 9.4 with appropriate sampling weights to account for the complex survey design, stratification, and cluster variable. A total of 2,518 adolescents was included in the analysis, representing 2.5 million Korean adolescents. The mean± standard deviation participant age was 15.3±1.7 years, and 55.3% were male. The number of participants with active tobacco smoke exposure was 283 (11.2%), passive tobacco smoke exposure was 145 (5.8%), and no smoke exposure was 2,090 (83.0%). Analysis of the 2,518 urine-cotinine-verified participants showed that tobacco smoke exposure had a significant effect on EBP: with an odds of elevated blood pressure of 3.00 (95% confidence interval [CI], 1.14 to 7.89). The odds of hypertension were 3.61 (95% CI, 1.13 to 11.49) in the active smoking group compared with the no tobacco exposure group after adjustment for potential confounders. It is necessary to present a range of public health plans to reduce tobacco exposure that affects adolescents' blood pressure, and further research with a larger number of participants using urine cotinine as a biomarker is needed.

Gender differences in the associations between tobacco smoke exposure and depressive symptoms among U.S. adults: NHANES 2007–2018

BackgroundFindings concerning gender differences in the associations between tobacco smoke exposure (TSE) and depression are inconsistent. This study aimed to investigate the gender-specific associations between active and passive TSE with depressive symptoms in a large, nationally representative sample of U.S. adults. MethodsData were from 27,175 adults aged ≥20 years in the 2007–2018 National Health and Nutrition Examination Survey (NHANES). Depressive symptoms were assessed using the Patient Health Questionnaire-9 (PHQ-9). Multivariable logistic regression was used to adjust for possible confounders. Whether the TSE-depression relationships may differ by age, race/ethnicity, socioeconomic status, body mass index (BMI), and self-reported health status was examined. ResultsAfter adjustment for lifestyle- and health-related variables, no significant associations between active (OR, 1.16 [95% CI, 0.87–1.55]) and passive TSE (OR, 0.84 [95% CI, 0.59–1.19]) and depressive symptoms were found among men. Among women, active TSE was associated with depressive symptoms (OR, 1.90 [95% CI, 1.51–2.39]), while the association for passive TSE was nonsignificant (OR, 1.11 [95% CI, 0.91–1.34]) after adjusting for lifestyle- and health-related variables. Interaction and subgroup analyses showed that self-reported health status could modify the relationship between passive TSE and depressive symptoms among women. Furthermore, a dose-response relationship between serum cotinine and depressive symptoms was found in women, but not in men. ConclusionsThis study suggests a stronger TSE-depression association in women than in men. Understanding these gender-specific patterns and identifying the potential moderators of such relationships will enable better targeting of public health interventions.

Prenatal tobacco smoke exposure and neurological impairment at 10years of age among children born extremely preterm: a prospective cohort.

To determine the association between prenatal tobacco smoke exposure and neurological impairment at 10years of age among children born extremely preterm (<28weeks of gestation). The Extremely Low Gestational Age Newborn (ELGAN) Study, a prospective cohort. Ten-year follow-up of extremely preterm infants born at 14 US hospitals between 2002 and 2004. Prenatal tobacco smoke exposure was defined as a mother's report at enrolment of active (i.e. maternal) and passive smoking during pregnancy. Poisson regression with generalized estimating equations was used. Models adjusted for mother's age, race/ethnicity, education, insurance, pre-pregnancy body mass index, US region, multiple gestation and infant's sex; and in sensitivity analysis, gestational age at delivery and clinical subtype of preterm birth, given their classification as intermediate and non-confounding variables. Neurological impairment at 10years, epilepsy, cerebral palsy and cognitive impairment. Of 1200 ELGAN study survivors, 856 were assessed at 10years of age with neurological outcomes, of whom 14% (118/856) had active tobacco exposure during pregnancy and 24% (207/852) had passive tobacco exposure. Compared with children who were not exposed prenatally to tobacco, children exposed to active tobacco use during pregnancy had a higher risk of epilepsy (14% versus 5%; adjusted relative risk: 1.68, 95% CI 1.45-1.92). This risk remained after adjustment for gestational age at delivery and clinical subtype of preterm birth. Prenatal tobacco smoke exposure was not associated with other assessed neurological outcomes, including cerebral palsy and multiple measures of cognitive impairment. Among children born extremely preterm, prenatal active tobacco smoke exposure was associated with an increased risk of epilepsy at 10years of life. Among infants born before 28weeks of gestation, prenatal active tobacco smoke exposure was associated with an increased risk of epilepsy at 10years of life.

Prenatal tobacco exposure and ADHD symptoms at pre-school age: the Hokkaido Study on Environment and Children\u2019s Health

BackgroundThere have been inconsistent findings reported on maternal passive smoking during pregnancy and child risk of ADHD. In this study, ADHD symptoms at pre-school age children in association with prenatal passive and active tobacco smoke exposure determined by maternal plasma cotinine levels in the third trimester were investigated.MethodsThis was a follow-up study of the birth cohort: the Hokkaido Study on Environment and Children’s Health. Children whose parents answered Strengths and Difficulties Questionnaire (SDQ) to identify child ADHD symptoms (hyperactivity/inattention and conduct problems) and total difficulties at age 5 years with available maternal plasma cotinine level at the third trimester were included (n = 3216). Cotinine levels were categorized into 4 groups; ≦ 0.21 ng/ml (non-smoker), 0.22–0.51 ng/ml (low-passive smoker), 0.52–11.48 ng/ml (high-passive smoker), and ≧ 11.49 ng/ml (active smoker).ResultsMaternal cotinine levels of active smokers were significantly associated with an increased risk of total difficulties (OR = 1.67) and maternal low- and high-passive smoking also increased the risk (OR = 1.11, 1.25, respectively) without statistical significance. Similarly, maternal cotinine levels of active smokers were associated with an increased risk of hyperactivity/inattention (OR = 1.49). Maternal low- and high-passive smoking and active smoking increased the risk of hyperactivity/inattention (OR = 1.45, 1.43, and OR = 1.59, respectively) only in boys.ConclusionOur findings suggested that maternal active smoking during pregnancy may contribute to the increased risk of child total difficulties and hyperactivity/inattention at pre-school age. Pregnant women should be encouraged to quit smoking and avoid exposure to tobacco smoke.

Active Tobacco Smoke Exposure in Utero and Concentrations of Hepcidin and Selected Iron Parameters in Newborns.

The aim of this study was to assess the influence of active tobacco smoke exposure in utero on the concentration of hepcidin and selected iron markers in umbilical cord blood and to evaluate the relationships between these parameters. Newborns of smoking mothers had significantly lower concentrations of serum hepcidin (p < 0.001), iron, and ferritin (p = 0.043; p = 0.042, respectively), but higher levels of erythropoietin (EPO, p < 0.001) and soluble transferrin receptor (sTfR, p = 0.011) compared with newborns of non-smoking women. Negative correlations between cotinine and the number of cigarettes smoked per day with hepcidin serum level (r = −0.33, p = 0.033, r = −0.32, p = 0.041, respectively) and EPO (r = 0.47, p = 0.002; r = 0.46, p = 0.003, respectively) were found. Univariate analysis defined for the whole group of children revealed significant associations between the concentration of hepcidin and other iron status parameters. In the models estimated separately for smokers and non-smokers, we found relations between the level of hepcidin and erythropoietin (B = −0.23, p = 0.004; B = −0.46, p = 0.01, respectively). In the multivariate regression model, a negative association between hepcidin and EPO concentrations in the whole group of newborns (β = −0.53; p = 0.001) and in the group of smokers (β = −0.57; p = 0.011) was confirmed. The present study shows significant relations between smoking during pregnancy and hepcidin levels in children born at term. Decreased cord serum concentrations of hepcidin associated with high erythropoietin levels suggest induced fetal erythropoiesis, probably due to the hypoxic effects imposed by maternal smoking.

Tobacco Smoke Exposure Association With Lipid Profiles and Adiposity Among U.S. Adolescents

PurposeWe investigated the association between tobacco smoke exposure (TSE) as measured by serum cotinine and lipoprotein cholesterols and adiposity in adolescents. MethodsWe performed a secondary analysis of 1999–2012 National Health and Nutrition Examination Survey data including participants 12–19 years old. We examined TSE: unexposed (<.05 ng/mL), passively exposed (.05–2.99 ng/mL), and actively exposed (≥3 ng/mL); lipid profiles: total cholesterol, high-density lipoprotein cholesterol (HDL-C), non-HDL-C, low-density lipoprotein cholesterol (LDL-C), and triglycerides; and adiposity: body mass index z-score (BMIZ), waist circumference (WC), and waist-to-height ratio (WHtR). Covariates were age, sex, race/ethnicity, income, diet, and physical activity. Multiple regression models were used to assess the association between TSE and lipid profile variables separately, and then TSE and adiposity measures separately, adjusting for covariates. We performed logistic regression to examine the association of TSE with body mass index and WHtR classifications. ResultsOf the 11,550 participants, 41.7% were unexposed to tobacco smoke, 40.5% were passively exposed, and 17.8% were actively exposed. Compared with unexposed, participants with active TSE had lower total cholesterol, lower HDL-C, and higher triglycerides; higher BMIZ, higher WC, and higher WHtR; participants with passive TSE had lower HDL-C, higher total cholesterol, and higher LDL-C; higher BMIZ, higher WC, and higher WHtR. Participants actively exposed were at increased odds of being obese or WHtR ≥.65, and those passively exposed were at increased odds of being overweight, obese, or WHtR ≥.65. ConclusionsActive TSE and passive TSE are differentially associated with factors within the lipid profile and adiposity, independent of covariates. TSE prevention efforts should start as early as childhood and continue throughout adolescence and adulthood.

The association between passive and active tobacco smoke exposure and child weight status among Spanish children.

To assess the impact of passive and active tobacco smoke exposure, both pre- and postnatally, on child body mass index (BMI) and overweight. Pregnant women were enrolled into the Spanish INMA prospective birth cohort during 1997 to 2008. Tobacco smoke exposure was assessed by questionnaire and corroborated by pre- and postnatal cotinine measurements. Children were followed up until 4 years in newer subcohorts (N = 1866) and until 14 years in one older subcohort (N = 427). Child age- and sex-specific BMI Z-scores were calculated, and generalized estimating equations were used to model their relationship with repeated measures of tobacco smoke exposure. Associations between prenatal passive exposure to tobacco smoke (adjusted β = 0.15, 95% CI: 0.05-0.25) and active maternal smoking (adjusted β = 0.20, 95% CI: 0.08-0.33) and child zBMI up to 4 years were observed. Stronger associations were observed in the older subcohort between both prenatal and child passive smoke exposure and zBMI up to 14 years. Evidence for an effect of both passive and maternal active smoking on child postnatal growth has been provided. Although residual confounding cannot be completely ruled out, associations were robust to adjustment for a range of lifestyle factors.

Serum cotinine and whole blood folate concentrations in pregnancy

PurposePrenatal tobacco smoke exposure may be associated with low maternal folate levels that increase the risk of adverse infant and child health outcomes by reducing folate availability during fetal development. MethodsUsing data from the Health Outcomes and Measures of the Environment Study, we examined the relationship between secondhand or active tobacco smoke exposure and whole blood folate concentrations in pregnant women from Cincinnati, Ohio (n = 362) at approximately 16-week gestation. We used multivariable linear regression to examine the association between continuous or categorical serum cotinine levels and whole blood folate levels, adjusting for sociodemographic, dietary, and perinatal variables. ResultsAfter adjustment for potential confounders, an interquartile range increases in serum cotinine concentration (0.012–0.224 ng/mL) was suggestively associated with decreased whole blood folate levels (β, −23 nmol/L; 95% confidence interval (CI), −49, 3; P value = .08). Compared with unexposed women, reductions in mean whole blood folate were observed among active smokers (β, −94, 95% CI, 195, 6 nmol/L; P value = .40); smaller reductions were observed among women with secondhand exposure (β, 26; CI, 84, 32 nmol/L; P value = .07). ConclusionsConsistent with prior studies, active smoking was associated with reduced whole blood folate levels among these pregnant women. Secondhand tobacco smoke exposures were associated with small and imprecise reductions in whole blood folate levels.

A prospective cohort study of biomarkers of prenatal tobacco smoke exposure: the correlation between serum and meconium and their association with infant birth weight

BackgroundThe evaluation of infant meconium as a cumulative matrix of prenatal toxicant exposure requires comparison to established biomarkers of prenatal exposure.MethodsWe calculated the frequency of detection and concentration of tobacco smoke metabolites measured in meconium (nicotine, cotinine, and trans-3'-hydroxycotinine concentrations) and three serial serum cotinine concentrations taken during the latter two-thirds of pregnancy among 337 mother-infant dyads. We estimated the duration and intensity of prenatal tobacco smoke exposure using serial serum cotinine concentrations and calculated geometric mean meconium tobacco smoke metabolite concentrations according to prenatal exposure. We also compared the estimated associations between these prenatal biomarkers and infant birth weight using linear regression.ResultsWe detected nicotine (80%), cotinine (69%), and trans-3'-hydroxycotinine (57%) in most meconium samples. Meconium tobacco smoke metabolite concentrations were positively associated with serum cotinine concentrations and increased with the number of serum cotinine measurements consistent with secondhand or active tobacco smoke exposure. Like serum cotinine, meconium tobacco smoke metabolites were inversely associated with birth weight.ConclusionsMeconium is a useful biological matrix for measuring prenatal tobacco smoke exposure and could be used in epidemiological studies that enroll women and infants at birth. Meconium holds promise as a biological matrix for measuring the intensity and duration of environmental toxicant exposure and future studies should validate the utility of meconium using other environmental toxicants.

Lung Cancer in Chinese Women: Evidence for an Interaction between Tobacco Smoking and Exposure to Inhalants in the Indoor Environment

BackgroundEpidemiologic data suggest that Chinese women have a high incidence of lung cancer in relation to their smoking prevalence. In addition to active tobacco smoke exposure, other sources of fumes and airborne particles in the indoor environment, such as cooking and burning of incense and mosquito coils, have been considered potential risk factors for lung cancer.ObjectivesWe used a case–control study to explore effects of inhalants from combustion sources common in the domestic environment on lung cancer and their modification by active tobacco smoking.MethodsWe analyzed 703 primary lung cancer cases and 1,578 controls. Data on demographic background and relevant exposures were obtained by face-to-face interviews in the hospital.ResultsWe observed a positive relationship with daily exposure to incense or mosquito coils and to cooking fumes only among smokers, and no association among lifetime nonsmokers. Interactions between smoking and frequency of cooking, or exposure to incense or mosquito coils were statistically significant and consistent with synergistic effects on lung cancer. The odds ratio (OR) comparing smokers without daily incense or mosquito coil exposure with nonsmokers without daily exposure was 2.80 [95% confidence interval (CI), 1.86–4.21], whereas the OR comparing smokers with daily exposure to the same referent group was 4.61 (95% CI, 3.41–6.24). In contrast, daily exposure to incense or mosquito coils was not associated with lung cancer among nonsmokers (OR = 0.91; 95% CI, 0.72–1.16). We observed the same pattern of associations for smokers without (OR = 2.31; 95% CI, 1.52–3.51) and with (OR = 4.50; 95% CI, 3.21–6.30) daily cooking exposure compared with nonsmokers, with no evidence of an association with daily cooking exposure among nonsmokers.ConclusionOur results suggest that active tobacco smoking not only is an important risk factor for development of lung cancer, but also may cause smokers to be more susceptible to the risk-enhancing effects of other inhalants.

Lifetime tobacco smoke exposure and breast cancer incidence

We analyzed data from a case-control study to assess the association between lifetime tobacco smoke exposure and breast cancer incidence. Incident breast cancer cases were identified in the Massachusetts Cancer Registry and population controls were sampled from state Medicare lists and driver's license rosters. Demographic, lifestyle, medical history, reproductive history, and passive and active smoking exposure variables were assessed by telephone interview. We defined passive and active tobacco smoke exposure categories reflective of lifetime exposure patterns, and compared breast cancer risk among these groups while adjusting for age, body mass index, menopausal status, parity, alcohol consumption, and family history of breast cancer. We also adjusted passive smoking associations for active smoking status and vice versa. We observed no association between ever being passively exposed to tobacco smoke and risk of incident breast cancer (adjusted OR: 1.2; 95% CI: 0.8, 1.8) nor between active smoking and breast cancer (adjusted OR for [23 pack-years compared to nonsmokers: 0.9; 95% CI: 0.7, 1.3). Null effects persisted in finer categorizations of active and passive exposure. We observed no causal associations between active or passive tobacco smoke exposures and incident breast cancer, consistent with results from most prospective cohort studies.