Cotinine concentrations in maternal serum and amniotic fluid during pregnancy and risk of testicular germ cell cancer in the offspring: A prospective nested case-control study.

Maternal smoking in pregnancy may increase the risk of testicular germ cell cancer (TGCC) in offspring, but current evidence remains inconclusive. We performed a nested case-control study using cotinine measurements in maternal serum and amniotic fluid as a biomarker for tobacco exposure during pregnancy. A total of 654 males with maternal serum (n = 359, ncases/controls = 71/288) and/or amniotic fluid (n = 295, ncases/controls = 66/229) samples were included. Data on TGCC diagnoses and relevant covariates were derived from nationwide Danish health registries. Cotinine was quantified by liquid chromatography tandem mass spectrometry. An adapted cox regression model estimated the risk of TGCC considering active and inactive tobacco use defined according to cotinine concentrations of <, ≥15 ng/ml. Overall, the concentrations of cotinine were comparable in maternal serum and amniotic fluid (medianserum/amniotic fluid : 2.1/2.6 ng/ml). A strong statistically significant correlation was detected in 14 paired samples (Spearman rho: 0.85). Based on maternal serum cotinine concentrations, exposure to active tobacco use was not associated with risk of TGCC in offspring (HR 0.88, 95% CI 0.51; 1.52). Similarly, based on amniotic fluid cotinine concentrations, exposure to active tobacco use was not associated with risk of TGCC (HR 1.11, 95% CI 0.64; 1.95). However, different risks were observed for seminomas and nonseminomas in both matrices, but none were statistically significant. Our findings did not provide convincing evidence supporting that exposure to tobacco during pregnancy is associated with TGCC.

The impact of maternal smoking during pregnancy and the age of smoking initiation on incident dementia: A prospective cohort study.

INTRODUCTION: The impact of early-life tobacco exposure on dementia has remained unknown. METHODS: Using the UK Biobank, the associations of maternal smoking during pregnancy (MSDP) and age of smoking initiation (ASI) with the onset time of all-cause dementia were estimated with accelerated failure time models. The effects of MSDP and ASI on brain structure and their genetic correlation to Alzheimer's disease (AD) were analyzed. A Mendelian randomization (MR) analysis was conducted. RESULTS: The time ratios for smokers starting in childhood, adolescence, and adulthood (vs never smokers) were 0.87 (0.76 to 0.99), 0.92 (0.88 to 0.96), and 0.95 (0.89 to 1.01). MSDP and smoking in adolescence altered many brain regions, including the hippocampus. In genetic analysis, MSDP was genetically and causally linked to AD, and a younger ASI was genetically correlated to a higher AD risk. DISCUSSION: Early-life smoking accelerated dementia onset and was genetically correlated to AD. MSDP demonstrated genetic and causal linkage to AD risks. HIGHLIGHTS: Unlike the commonly used Cox proportional hazards model, this article uses a parametric survival analysis method - the accelerated failure model - to explore the relationship between exposure to onset time. It can be used as an alternative method when the proportional hazards assumption is not met. Genetic analyses including genetic correlation study and MR analysis and brain structure analyses were conducted to support our findings and explore the potential mechanisms. The study reveals the relationship between different smoking initiation periods and the onset time of dementia and shows that earlier smoking exposure has a more significant impact on dementia. It emphasizes the importance of preventing early smoking. In the future, more research focusing on the relationship between early exposure and dementia is called for to provide more detailed prevention measures for dementia that cover all age groups.

Associations between community-level patterns of prenatal alcohol and tobacco exposure on brain structure in a non-clinical sample of 6-year-old children: a South African pilot study.

The current small study utilised prospective data collection of patterns of prenatal alcohol and tobacco exposure (PAE and PTE) to examine associations with structural brain outcomes in 6-year-olds and served as a pilot to determine the value of prospective data describing community-level patterns of PAE and PTE in a non-clinical sample of children. Participants from the Safe Passage Study in pregnancy were approached when their child was ∼6 years old and completed structural brain magnetic resonance imaging to examine with archived PAE and PTE data (n = 51 children-mother dyads). Linear regression was used to conduct whole-brain structural analyses, with false-discovery rate (FDR) correction, to examine: (a) main effects of PAE, PTE and their interaction; and (b) predictive potential of data that reflect patterns of PAE and PTE (e.g. quantity, frequency and timing (QFT)). Associations between PAE, PTE and their interaction with brain structural measures demonstrated unique profiles of cortical and subcortical alterations that were distinct between PAE only, PTE only and their interactive effects. Analyses examining associations between patterns of PAE and PTE (e.g. QFT) were able to significantly detect brain alterations (that survived FDR correction) in this small non-clinical sample of children. These findings support the hypothesis that considering QFT and co-exposures is important for identifying brain alterations following PAE and/or PTE in a small group of young children. Current results demonstrate that teratogenic outcomes on brain structure differ as a function PAE, PTE or their co-exposures, as well as the pattern (QFT) or exposure.

Demystifying the impact of prenatal tobacco exposure on the placental immune microenvironment: Avoiding the tragedy of mending the fold after death.

Prenatal tobacco exposure (PTE) correlates significantly with a surge in adverse pregnancy outcomes, yet its pathological mechanisms remain partially unexplored. This study aims to meticulously examine the repercussions of PTE on placental immune landscapes, employing a coordinated research methodology encompassing bioinformatics, machine learning and animal studies. Concurrently, it aims to screen biomarkers and potential compounds that could sensitively indicate and mitigate placental immune disorders. In the course of this research, two gene expression omnibus (GEO) microarrays, namely GSE27272 and GSE7434, were included. Gene set enrichment analysis (GSEA) and immune enrichment investigations on differentially expressed genes (DEGs) indicated that PTE might perturb numerous innate or adaptive immune-related biological processes. A cohort of 52 immune-associated DEGs was acquired by cross-referencing the DEGs with gene sets derived from the ImmPort database. A protein-protein interaction (PPI) network was subsequently established, from which 10 hub genes were extracted using the maximal clique centrality (MCC) algorithm (JUN, NPY, SST, FLT4, FGF13, HBEGF, NR0B2, AREG, NR1I2, SEMA5B). Moreover, we substantiated the elevated affinity of tobacco reproductive toxicants, specifically nicotine and nitrosamine, with hub genes through molecular docking (JUN, FGF13 and NR1I2). This suggested that these genes could potentially serve as crucial loci for tobacco's influence on the placental immune microenvironment. To further elucidate the immune microenvironment landscape, consistent clustering analysis was conducted, yielding three subtypes, where the abundance of follicular helper T cells (p < 0.05) in subtype A, M2 macrophages (p < 0.01), neutrophils (p < 0.05) in subtype B and CD8+ T cells (p < 0.05), resting NK cells (p < 0.05), M2 macrophages (p < 0.05) in subtype C were significantly different from the control group. Additionally, three pivotal modules, designated as red, blue and green, were identified, each bearing a close association with differentially infiltrated immunocytes, as discerned by the weighted gene co-expression network analysis (WGCNA). Functional enrichment analysis was subsequently conducted on these modules. To further probe into the mechanisms by which immune-associated DEGs are implicated in intercellular communication, 20 genes serving as ligands or receptors and connected to differentially infiltrating immunocytes were isolated. Employing a variety of machine learning techniques, including one-way logistic regression, LASSO regression, random forest and artificial neural networks, we screened 11 signature genes from the intersection of immune-associated DEGs and secretory protein-encoding genes derived from the Human Protein Atlas. Notably, CCL18 and IFNA4 emerged as prospective peripheral blood markers capable of identifying PTE-induced immune disorders. These markers demonstrated impressive predictive power, as indicated by the area under the curve (AUC) of 0.713 (0.548-0.857) and 0.780 (0.618-0.914), respectively. Furthermore, we predicted 34 potential compounds, including cyclosporine, oestrogen and so on, which may engage with hub genes and attenuate immune disorders instigated by PTE. The diagnostic performance of these biomarkers, alongside the interventional effect of cyclosporine, was further corroborated in animal studies via ELISA, Western blot and immunofluorescence assays. In summary, this study identifies a disturbance in the placental immune landscape, a secondary effect of PTE, which may underlie multiple pregnancy complications. Importantly, our research contributes to the noninvasive and timely detection of PTE-induced placental immune disorders, while also offering innovative therapeutic strategies for their treatment.

Cigarette smoking history (personal and secondary childhood exposure) in non-cluster headache trigeminal autonomic cephalalgias: A clinic based study.

OBJECTIVE: To look at cigarette smoking history (personal and secondary exposure as a child) in non-cluster headache trigeminal autonomic cephalalgias seen at a headache clinic and to determine smoking exposure prevalence utilizing previously published data. METHODS: Retrospective chart review and PubMed/Google Scholar search. RESULTS: Forty-eight clinic patients met ICHD-3 criteria for non-cluster headache trigeminal autonomic cephalalgias. Four had paroxysmal hemicrania, 75% were smokers and secondary exposure was noted in all. 16 patients had short lasting unilateral neuralgiform headache attacks with conjunctival injection and tearing (SUNCT) or short lasting unilateral neuralgiform headache attacks with autonomic symptoms (SUNA), 12.5% were smokers and secondary exposure was noted in 91%. Twenty-eight patients had hemicrania continua, 21% were smokers and secondary exposure was found in 62.5%.Since 1974 there have been 88 paroxysmal hemicrania, 50 SUNCT or SUNA and 89 hemicrania continua patients with a documented smoking exposure history. From current data and previous studies, a smoking history was noted in 60% paroxysmal hemicrania, 18% SUNCT and SUNA and 21% hemicrania continua patients. CONCLUSION: A cigarette smoking history appears to be connected to paroxysmal hemicrania (personal and secondary exposure) and possibly to SUNCT/SUNA (secondary) and hemicrania continua (secondary).

Tobacco Exposure During Pregnancy and Infections in Infants up to 1 Year of Age: The Japan Environment and Children's Study.

BACKGROUND: Tobacco exposure during pregnancy is associated with several adverse outcomes in infants. We investigated the association between tobacco exposure during pregnancy (both active and second-hand) and various infections in infants up to 1 year. METHODS: This prospective cohort study used a fixed dataset (jecs-an-20180131) from the Japan Environment and Children's Study of registered births in Japan during 2011-2014 that included 104,065 fetal records from enrolled pregnant women. Based on the participants' responses to the questionnaire on smoking status, mothers were first divided into "never smoked," "quit smoking," and "current smoker" groups and then into "no second-hand smoking (SHS)" and "SHS" groups. Infectious diseases included central nervous system infection, otitis media (OM), upper respiratory tract infection (URTI), lower respiratory tract infection (LRTI), gastroenteritis (GI), and urinary tract infection. Adjusted odds ratios (aORs) and 95% confidence intervals (CIs) were calculated using logistic regression analysis and adjusted for maternal, socioeconomic, and postnatal confounding factors. RESULTS: Among the 73,205 newborns enrolled, multivariable analysis revealed that the aOR of LRTI and GI was 1.20 (95% CI, 1.07-1.33) and 1.18 (95% CI, 1.04-1.35), respectively, for the "current smoker with/without SHS" group compared with the "never smoked without SHS" group. "Quit smoking without SHS" was not associated with the risk of LRTI. SHS was associated with an increased risk of OM, URTI, LRTI, and GI, especially with LRTI and GI. CONCLUSION: Exposure to tobacco smoke during pregnancy was associated with an increased risk of OM, URTI, LRTI, and GI in infants during their first year of life.

Associations between prenatal alcohol and tobacco exposure on Doppler flow velocity waveforms in pregnancy: a South African study.

BACKGROUND: The negative impact of prenatal alcohol and tobacco exposure (PAE and PTE) on fetal development and birth outcomes are well described, yet pathophysiologic mechanisms are less clear. Our aim was to investigate (1) the associations between quantity, frequency and timing (QFT) of PAE and PTE with blood flow velocities in arteries of the fetal-placental-maternal circulation and (2) the extent to which combined effect of QFT of PAE and/or PTE and Doppler flow velocity waveforms (FWV) predict infant birth weight. METHODS: The Safe Passage Study is a cohort based in urban Cape Town, South Africa. Recruitment occurred between 2007 and 2015. Information on QFT of PAE and PTE was collected prospectively at up to 4 occasions during pregnancy using a modified Timeline Follow-Back approach. Ultrasound examinations consisted of Doppler flow velocity waveforms of the uterine, umbilical (UA) and fetal middle cerebral arteries for the pulsatility index (PI) at 20-24 and 34-38 weeks. Exclusion criteria included: twin pregnancies, stillbirths, participants exposed to other drugs. The sample was divided into three groups (controls, PAE and PTE) and included 1396 maternal-fetal-dyads assessed during the second trimester; 1398 assessed during the third trimester. RESULTS: PTE was associated with higher UA PI values in second and third trimesters (p < 0.001), compared to the PAE and control group. The total amount of cigarettes smoked during pregnancy was positively correlated with UA PI values (r = 0.087, p < 0.001). There was a positive correlation between cigarettes smoked per day in trimester one (r = 0.091, p < 0.01), and trimester two (r = 0.075, p < 0.01) and UA PI (in trimester two), as well as cigarettes smoked per day in trimester two (r = 0.058, p < 0.05) and trimester three (r = 0.069, p < 0.05) and the UA PI in trimester three. Generalized additive models indicated that PAE in trimester two, PTE in trimester one and Doppler FWV in trimester three were significant predictors of birth weight in this sample. CONCLUSION: In our study, PTE in trimesters two and three resulted in increased vascular resistance of the placenta. These findings highlight nuance in associations between PAE, PTE and blood flow velocities in arteries of the fetal-placental-maternal circulation and birth weight, suggesting that quantity and timing are important factors in these relationships.

Epidemiology of Lung Cancer Mortality in Spain: Updated Information (1982-2021) and Predictions up to 2046.

BACKGROUND: Patterns of lung cancer (LC) mortality are important for planning health services and resource management. OBJECTIVES: We aimed to provide updated information (1982-2021) and project (LC) mortality rates in Spain (2022-2046). METHOD: We analysed data from the Spanish National Statistics Institute about mortality in LC (1982-2021), and we made predictions for the period 2022-2046. RESULTS: In 2021, a total of 22,413 people died of LC, and for the period 2042-2046, the projected annual average was 25,549 deaths. In males, age-standardised mortality rates (ASMR) (overall) after an initial period of increase (1982-1996, 2.2%) declined until 2021 (-1.4% per year), and this decline is expected to continue in the future (-1.9% per year during the period 2022-2046), although the projected decline is slightly higher (-2.0% during the period 2022-2046). In men, ASMR (all ages) after an initial period of increase (1982-1996, 2.2%) declined until 2021 (-1.4% per year), and this decline is expected to continue in the future during the period 2022-2046. In women, both the overall and truncated rates (35-64) increase during the period 1982-2021 (4.1% and 6.0% per year, respectively), and projected rates showed that both will decrease during the period 2022-2046, although more markedly in the truncated rates (-1.9% per year) than in the overall rates (-0.5% per year). CONCLUSIONS: Our projections show the magnitude of a steady upward trend in LC mortality among women in Spain that appears to be beginning to reverse from the current decade (similar to that observed for incidence).

Long-term impact of tobacco exposure during pregnancy on children's psychomotor development.

BACKGROUND: Both active and second-hand smoking (SHS) can cause complications during pregnancy and after delivery. This study aimed to assess how tobacco exposure (active and passive) during the fetal period could impact the psychomotor development of children when they attain the age of 3-6 years. METHODS: The study included 160 mothers and their 3-6 year-old children. Two research groups were set up of children born to active or SHS mothers during the period when they were pregnant and a control group of children of non-smoking mothers. The parameters of the psychomotor development of the children were measured using the Age & Stage Questionnaires 3® (ASQ-3). RESULTS: Children, whose mothers were smokers themselves or who were exposed to SHS during the period of pregnancy had an average psychomotor development score of 221 points versus 243.5 points in the control group. Twenty-six percent had delays (near or under the cut-off scores) in one of the assessed psychomotor areas and 60% had two or more psychomotor delays; 36% of children whose mothers were not exposed to smoking during pregnancy had normal psychomotor development and only 34% presented multiple psychomotor delays. CONCLUSIONS: Fetuses exposed to tobacco are more likely to achieve a psychomotor development in the 'monitor' and 'fail' areas compared to the non-exposed control group. The children exposed to smoking during their fetal development should be considered as a group at risk of developmental delays, therefore they should be closely monitored and supported by caregivers and developmental pediatricians.

The impact of tobacco smoking on survival of patients with oral squamous cell carcinoma: a population-based retrospective study.

BACKGROUND: This article aims to evaluate the impact of smoking status, accumulated tobacco exposure (ATE), and smoking cessation on overall- and disease-free survival (OS and DFS) of patients with oral squamous cell carcinoma (OSCC). MATERIAL AND METHODS: Patients with primary OSCC treated with curative intent between 2000 and 2019 in Copenhagen were included (n = 1808). Kaplan-Meier curves and multivariable Cox regression analyses were performed to compare the survival of patients with different smoking history. Interactions between ATE and (A) tumor subsite and (B) excessive alcohol consumption (EAC) on the survival were evaluated using multivariable Cox regression analyses with interaction terms. RESULTS: We included 1717 patients with known smoking status (62.8% males, median age: 64 years (IQR: 57-71 years)), who had a 5-year OS of 53.7% (95%CI: 49.8%-57.9%). Based on fully adjusted multivariable Cox regression analyses, significantly elevated hazard ratios (HRs) for OS and DFS were identified for current, but not former smokers, compared to never-smokers. An approximately linear relationship between continuous ATE and survival estimates was identified. ATE analyzed as a categorical variable showed significantly elevated HRs for OS of patients with all categories (060 PYs), however only for DFS of patients with >60 PYs, compared to 0 PYs. Furthermore, an unfavorable long-term prognosis was evident after >3.5 (OS) and >2.5 (DFS) years from diagnosis for patients who continued smoking compared to patients with smoking cessation at diagnosis. The survival estimates of patients with different tumor subsite and alcohol consumption differed with increasing ATE. CONCLUSION: Tobacco smoking (assessed as smoking status and ATE) was associated with inferior survival (OS and DFS) among patients with OSCC. Unfavorable long-term prognosis was significant for patients who continued smoking compared to patients with smoking cessation at diagnosis. The impact of ATE on survival of patients with OSCC may depend on the tumor subsite and/or alcohol consumption.

Alcohol consumption and tobacco exposure among pregnant women in Ibadan, Nigeria.

BACKGROUND: Alcohol consumption and tobacco exposure during pregnancy are hazardous behaviours which are increasing significantly in low and middle-income countries, including sub-Saharan Africa. However, they have received little attention in Nigeria's maternal health research and services. The prevalence, pattern and predictors of alcohol consumption and tobacco exposure among pregnant women in Ibadan, Nigeria, were investigated. METHODS: This is a part of a prospective cohort study among pregnant women in Ibadan, Nigeria (Ibadan Pregnancy Cohort Study (IbPCS), which investigated the associations between maternal obesity, lifestyle characteristics and perinatal outcomes in Ibadan. Alcohol consumption and tobacco exposure of 1745 pregnant women were assessed during enrollment by self-reports using an interviewer-administered questionnaire. Bivariate and multiple logistic regression analyses examined the associations at a 5% level of statistical significance. RESULTS: The prevalence of pre-pregnancy alcohol consumption and alcohol consumption during pregnancy were 551 (31.7%) and 222 (12.7%), respectively, i.e. (one in every eight pregnancies is exposed to alcohol). Palm wine (52%) and beer (12%) were the most common alcohol consumed among pregnant women. The predictors of alcohol consumption during were pre-pregnancy alcohol use [AOR = 10.72, 95% CI: 6.88-16.70) and religion i.e. Muslims were less likely to consume alcohol during pregnancy compared to Christians: [AOR = 0.60, 95% CI: 0.40-0.92). The prevalence of tobacco exposure in the index pregnancy was 64 (3.7%), i.e. one in every 27 pregnancies is exposed to tobacco. In contrast, cigarette smoking, second-hand smoke and smokeless tobacco were 0.4, 1.7 and 1.8%, respectively. Pre-pregnancy cigarette smoking was reported by 33(1.9%) and was the most significant predictor [AOR = 12.95; 95% CI: 4.93, 34.03) of tobacco exposure during pregnancy in our study population. CONCLUSIONS: Alcohol consumption and tobacco exposure are not uncommon and have been an ongoing but neglected threat to maternal and child health in Nigeria. Alcohol and tobacco control policy and programmes to prevent the use among pregnant and reproductive-age women in Nigeria should be implemented primarily during antenatal care.

Prenatal Exposure to Tobacco and Alcohol Alters Development of the Neonatal Auditory System.

Prenatal exposures to alcohol (PAE) and tobacco (PTE) are known to produce adverse neonatal and childhood outcomes including damage to the developing auditory system. Knowledge of the timing, extent, and combinations of these exposures on effects on the developing system is limited. As part of the physiological measurements from the Safe Passage Study, Auditory Brainstem Responses (ABRs) and Transient Otoacoustic Emissions (TEOAEs) were acquired on infants at birth and one-month of age. Research sites were in South Africa and the Northern Plains of the U.S. Prenatal information on alcohol and tobacco exposure was gathered prospectively on mother/infant dyads. Cluster analysis was used to characterize three levels of PAE and three levels of PTE. Repeated-measures ANOVAs were conducted for newborn and one-month-old infants for ABR peak latencies and amplitudes and TEOAE levels and signal-to-noise ratios. Analyses controlled for hours of life at test, gestational age at birth, sex, site, and other exposure. Significant main effects of PTE included reduced newborn ABR latencies from both ears. PTE also resulted in a significant reduction of ABR peak amplitudes elicited in infants at 1-month of age. PAE led to a reduction of TEOAE amplitude for 1-month-old infants but only in the left ear. Results indicate that PAE and PTE lead to early disruption of peripheral, brainstem, and cortical development and neuronal pathways of the auditory system, including the olivocochlear pathway.

Within- and between-family transactions of maternal depression and child engagement in the first 2 years of life: Role of prenatal maternal risk and tobacco use.

BACKGROUND: This study examined transactional associations among maternal depression, maternal sensitivity, and child engagement in the context of a low-income, diverse sample with maternal cigarette smoking during pregnancy (MSDP) as a moderator of these transactions. METHODS: A random-intercept cross-lagged panel model was used to investigate within- and between-family variability from infancy to toddlerhood. The sample included 247 mother-child dyads (47% girls; 51% African-American; 178 MSDP, 69 non-MSDP). Assessments were conducted once during each trimester of pregnancy and at 2, 9, 16, and 24 months of child ages. RESULTS: Between-family associations revealed that children exposed to higher levels of sensitive parenting across time had higher behavioral engagement from infancy to toddlerhood. At the within-family level, increased sensitive parenting at 9 months was predictive of increased child engagement at 16 months which in turn predicted increases in sensitive parenting at 24 months. Increased maternal depression was concurrently associated with lower maternal sensitivity at 2 months and lower child engagement at 16 months. Contrary to hypotheses, changes in maternal depression were not associated to changes in parenting or child engagement. These associations did not vary between prenatally smoking and nonsmoking mothers. However, there was significantly higher stability in maternal depression across time among nonsmoking mothers compared to those in the MSDP group. Additionally, increased maternal depression was related to lower-than-expected child engagement at 9 months only for the nonsmoking group. CONCLUSIONS: Results highlight transactional processes at the within-family level and the importance of timing for parent and child effects on transactional processes.

Third-hand exposure at homes: Assessment using salivary cotinine.

BACKGROUND/OBJECTIVES: While exposure to secondhand smoke (SHS) is a well-established problem, exposure to third-hand smoke (THS) is scanty known and needs to be studied. The objective of this work is to characterize salivary cotinine concentrations among people who self-reported exposure to SHS and THS at home. METHODS: Cross-sectional study of a representative sample (n = 736) of the adult population (≥16 years) from the city of Barcelona carried out in 2013-2014. A questionnaire on tobacco use and passive exposure was administered, and a saliva sample was collected for cotinine determination. For this study, the information of the non-smoker participants who provided saliva sample (n = 519) was used. The geometric means (GM) and geometric standard deviations (GSD) of the cotinine concentration were compared according to the type of self-reported exposure at home: (1) Not exposed to SHS or THS; (2) Exposed to SHS and THS; and (3) Only exposed to THS. We used log-linear models to compare the cotinine concentration of each exposed group with respect to the unexposed group, adjusting for sex, age, educational level, and tobacco exposure in other settings. RESULTS: The GM of the salivary cotinine concentration was 0.34 ng/ml (GSD = 0.16) among individuals reporting SHS and THS exposure, 0.22 ng/ml (GSD = 0.15) among those reporting only THS exposure and 0.11 ng/ml (GSD = 0.04) among those who declared not to be exposed to SHS nor THS (p-value for trend <0.001). The regression model showed a statistically significant increase in cotinine concentration among those exposed to SHS and THS (188% higher, 95% CI: 153%; 223%), and only exposed to THS (106% higher, IC95. %: 74.5%; 137.0%) when comparing with the unexposed group. No statistically significant differences in cotinine concentration were observed between those exposed to SHS and THS compared to the THS group (-25.8%, 95% CI: -69.5%; 17.9%). CONCLUSIONS/RECOMMENDATIONS: People exposed to third-hand smoke at home had quantifiable cotinine levels in saliva. No differences in cotinine levels were found between those exposed to second-hand and third-hand smoke at home. The reduction of exposure to third-hand smoke at home should be put into the agenda of tobacco control.

Association between environmental tobacco smoke exposure across the first four years of life and manifestation of externalizing behavior problems in school-aged children.

BACKGROUND: Extensive literature in human and animal models has documented an association between maternal smoking during pregnancy and externalizing behavior in offspring. It remains unclear; however, the extent to which postnatal environmental smoke exposure is associated with behavioral development, particularly for children whose mothers did not smoke during pregnancy. The present study examined whether magnitude of exposure to environmental smoke across the first four years of life demonstrated a linear association with later externalizing symptoms. METHODS: Exposure was quantified through salivary cotinine measured when children were 6, 15, 24, and 48 months of age, providing a more accurate quantification of realized exposure than can be estimated from parental report of cigarettes smoked. Data were available for n = 1,096 (50% male; 44% African American) children recruited for the Family Life Project, a study of child development in areas of rural poverty. RESULTS: Analyses indicate a linear association between cotinine and children's symptoms of hyperactivity and conduct problems. This association remained significant after controlling for family poverty level, parental education, parental history of ADHD, hostility, depression, caregiver IQ, and obstetric complications. Furthermore, this association was unchanged when excluding mothers who smoked during pregnancy from the model. CONCLUSIONS: Findings are consistent with animal models demonstrating an effect of environmental exposure to nicotine on ongoing brain development in regions related to hyperactivity and impulsivity, and highlight the importance of mitigating children's exposure to environmental smoke, including sources that extend beyond the parents.

Parental tobacco smoking and risk of childhood leukemia in Costa Rica: A population-based case-control study.

INTRODUCTION: The role of environmental and behavioral exposures on childhood leukemia etiology is poorly understood. We examined the association of maternal and paternal tobacco smoking at different time points with the risk of acute lymphoblastic leukemia (ALL) and acute myeloid leukemia (AML) in Costa Rican children. MATERIALS AND METHODS: We conducted a population-based case-control study on childhood leukemia in Costa Rica. Cases (n ALL = 252; n AML = 40) were diagnosed between 1995 and 2000 (aged <15 years at diagnosis) and identified from the Costa Rican Cancer Registry and the National Children's Hospital. A total of 578 frequency-matched population controls were sampled from the National Birth Registry. Parental tobacco smoking was assessed via face-to-face interviews. We used logistic regression models to examine the association of paternal and maternal tobacco smoking before conception, during pregnancy, and after birth with childhood ALL and AML risk, adjusted for child sex, birth year, maternal/paternal age, and parental education. RESULTS: Paternal smoking before conception, during pregnancy, and after birth was associated with an increased risk of childhood AML (Odds Ratio (OR): 2.51, 95% CI: 1.21-5.17; OR: 3.21, 95% CI: 1.56-6.60; and OR: 2.83, 95% CI: 1.36-5.90, respectively). Maternal smoking during pregnancy was also associated with a modest, but imprecise increase in AML risk. We observed null associations of maternal and paternal smoking with ALL in the offspring. CONCLUSION: Our results suggest an association between parental smoking and risk of AML, but not ALL, in Costa Rican children. These findings add to the established evidence of numerous health risks associated with smoking and highlight the potential harm of smoking during sensitive windows of the development of fetus and child.

A cross country comparison for the burden of cardiovascular disease attributable to tobacco exposure in China, Japan, USA and world.

BACKGROUND: Tobacco exposure (TE) is the major contributor for CVD mortality, but few published studies on CVD mortality attributable to TE have analyzed the potential reasons underlying long-term trends in China. Our studysought to find the potential reasons and compared CVD mortality attributable to TE in China, Japan, the United States of America (USA), and the world between 1990 and 2017. METHODS: The mortality data in China, Japan, the USA, and the world were obtained from Global Burden of Disease Study 2017(GBD 2017). Joinpoint regression was used to assess the trend magnitude and directions over time for CVD mortality, while the age-period-cohort method was used to analyzethe temporal trends of CVD mortality according to age, period, and cohort. RESULTS: A significant downward trend was found in the age-standardised mortality rate (ASMR) of CVD attributable to smoking in four regions. China had the smallest decline and the Chinese ASMR became the highest in 2017. All the annual net drifts in the four regions were negative and the local drifts were below zero. The longitudinal age curves of CVD mortality attributable to smoking increased in four regions,with China having the largest increase. The period or cohort RRs indicated a decline, and China had the smallest decline. The researchers further analyzed the IHD and stroke trends, finding that the morality and period or cohort RR of IHD in China was always at a high level. CONCLUSIONS: CVD mortality attributable to TE declined in four regions, and was highest in China. The proportion of IHD mortality attributable to TE was similar to stroke, which significantly changed the traditional cognition of CVD composition, but the control measure was not sufficient for IHD in China.

Does early maternal responsiveness buffer prenatal tobacco exposure effects on young children's behavioral disinhibition?

Children with prenatal tobacco exposure (PTE) exhibit early self-regulatory impairments, reflecting a life-course persistent propensity toward behavioral disinhibition. Previously, we demonstrated the protective role of parental responsiveness for reducing the risk of exposure-related disruptive behavior in adolescence. Here, we expanded this line of inquiry, examining whether responsiveness moderates the relation of PTE to a broader set of behavioral disinhibition features in early childhood and testing alternative diathesis-stress versus differential susceptibility explanatory models. PTE was assessed prospectively using interviews and bioassays in the Midwestern Infant Development Study (MIDS). Mother-child dyads (N = 276) were re-assessed at approximately 5 years of age in a preschool follow-up. We quantified maternal responsiveness and child behavioral disinhibition using a combination of directly observed activities in the lab and developmentally sensitive questionnaires. Results supported a diathesis-stress pattern. Children with PTE and less responsive mothers showed increased disruptive behavior and lower effortful control compared with children without PTE. In contrast, exposed children with more responsive mothers had self-regulatory profiles similar to their non-exposed peers. We did not observe sex differences. Findings provide greater specification of the protective role of maternal responsiveness for self-regulation in children with PTE and help clarify mechanisms that may underscore trajectories of exposure-related behavioral disinhibition.

Prenatal exposure to tobacco and marijuana and child autonomic regulation and reactivity: An analysis of indirect pathways via maternal psychopathology and parenting.

We examined a conceptual model for the associations of prenatal exposure to tobacco (PTE) and marijuana with child reactivity/regulation at 16 months of age. We hypothesized that PTE would be associated with autonomic reactivity and regulation that these associations would be indirect via maternal anger/hostility, depression/stress, or harsh parenting assessed at 2 months and that these effects would be most pronounced among children exposed to both tobacco and marijuana (PTME). Participants were 247 dyads (81 PTE, 97 PTME, and 69 nonexposed) who were followed up at 2 (N = 247) and 16 months (N = 238) of child age. Results from model testing indicated an indirect association between PTME and autonomic functioning during the second year of life, which was mediated by harsh parenting during caregiver-infant interactions. This study fills an important gap in the literature on PTE, PTME, and autonomic regulation during the toddler years, highlighting the role of maternal parenting as important intervening variables.

Longitudinal association between tobacco use and the onset of depressive symptoms among Swedish adolescents: the Kupol cohort study.

Tobacco use in adolescence has been linked to the onset of depressive symptoms, but results of previous studies are inconsistent. The aim of this study was to clarify if tobacco use during early adolescence may affect the short-term onset of depressive symptoms. The study is based on Swedish Kupol study (3959 students). Current cigarette smoking, snus use, and tobacco dependence were assessed using questionnaires at baseline and 1-year follow-up. Outcome was the onset of depressive symptoms measured with the CES-DC scale, using a cut-off ≥ 30 as threshold. Adjusted linear and logistic regression models were employed to calculate odds ratios (OR) and corresponding 95% confidence intervals (CI). CES-DC mean score at baseline was 14.3, higher in females than males (17.5 vs 10.9). The incidence of depressive symptoms at follow-up was 8.3%, greater in current than never smokers at baseline (13.7% vs 3.1%). Current cigarette smoking at the age of 13 years was strongly associated with the onset of depressive symptoms 1 year later, particularly in males (OR 12.7, 95% CI: 2.5-63.9), with a significant interaction between tobacco use and sex; feeling dependent on tobacco was also associated with depressive symptoms in males but not in females. Snus and overall tobacco use were not associated with the onset of depressive symptoms. Tobacco use during adolescence appears to influence the onset of depressive symptoms, with a stronger association in males than females. Pubertal maturation and sex-specific response patterns to the scale instrument may explain the moderating effect of sex.