Prenatal hazardous substance use and adverse birth outcomes

Objective: Assess the relative effects of a variety of illicit and licit drugs on risk for adverse birth outcomes. Methods: We used data from two large prospective investigations, and a novel analytic method, recursive partitioning class analysis to identify risk factors associated with preterm birth and delivering a small for gestational age infant. Results: Compared to cocaine and opiate non-users, cocaine users were 3.53 times as likely (95% CI: 1.65-7.56; p = 0.001) and opiate users 2.86 times as likely (95% CI: 1.11-7.36; p = 0.03) to deliver preterm. The odds of delivering a small for gestational age infant for women who smoked more than two cigarettes daily was 3.74, (95% CI: 2.47-5.65; p<0.0001) compared to women who smoked two or less cigarettes daily and had one previous child. Similarly, less educated, nulliparous women who smoked two or fewer cigarettes daily were 4.12 times as likely (95% CI: 2.04-8.34; p < 0.0001) to have a small for gestational age infant. Conclusions: Among our covariates, prenatal cocaine and opiate use are the predominant risk factors for preterm birth; while tobacco use was the primary risk factor predicting small for gestational age at delivery. Multi-substance use did not substantially increase risk of adverse birth outcomes over these risk factors.     

Comparative study of the main characteristics and composition of the mainstream smoke of ten cigarette brands sold in Spain

In this study 10 commercial top selling cigarette brands in Spain have been machine smoked and the mainstream smoke has been analyzed. Multifunctional analysis has been satisfactorily employed to correlate the effect of the main design features of the cigarettes including amount of tobacco, filter size or paper weight with the amount of smoked tobacco and with the ratio CO₂/CO. The composition of the vapor phase and that of the particulate matter have been analyzed. The particulate matter retained in the filter of the cigarettes has also been analyzed showing a distinct behavior of the compounds condensed in the cigarette filters and in the traps, related to their retention time. A general trend for the relative yield of some compounds in the different brands have been identified and confirmed by multifunctional analysis. Nevertheless, there are some noticeable compounds that behave differently in the different brands.     

Assessment of genotoxicity of waterpipe and cigarette smoking in lymphocytes using the sister‐chromatid exchange assay: A comparative study

Tobacco smoking is a major world health problem. Recently, waterpipe smoking has become more popular in many countries. Although the genotoxicity associated with cigarette smoking has been extensively investigated, studies evaluating such toxicity in waterpipe users are still lacking. In this study, we examined the genotoxicity of waterpipe smoking in lymphocytes compared with the genotoxicity of cigarette smoking. Genotoxicity was evaluated using the sister chromatid exchanges (SCEs) assay. Fifty waterpipe smokers and 18 healthy nonsmokers participated in this study. Additionally, 18 heavy cigarette smokers (CS) were recruited for comparison. The results show that waterpipe smoking and cigarette smoking significantly increase the frequencies of SCEs (P < 0.01) compared with those of nonsmokers, indicating the genotoxic effect of tobacco smoking. In addition, frequencies of SCEs were significantly higher among waterpipe smokers compared with CS (P < 0.01), indicating that waterpipe smoking is more genotoxic than cigarette smoking. Moreover, the frequency of SCEs increased with the extent of waterpipe use. In conclusion, waterpipe smoking is genotoxic to lymphocytes and the magnitude of its genotoxicity is higher than that induced by regular cigarette smoking. Environ. Mol. Mutagen., 2011. © 2010 Wiley‐Liss, Inc.     

Protective effect of melatonin on cigarette smoke‐induced restenosis in rat carotid arteries after balloon injury

Vascular restenosis after the interventional angioplasty remains the main obstacle to a favorable long‐term patency. Many researches suggest cigarette smoking is one of the most important causes of restenosis. This study was designed to investigate whether melatonin could protect against the cigarette smoke‐induced restenosis in rat carotid arteries after balloon injury. Three groups of male rats (normal condition, cigarette smoke exposed, cigarette smoke exposed, and melatonin injected) were used in this study. An established balloon‐induced carotid artery injury was performed, and the carotid arteries were harvested from these three groups 14 days later. The ratio of intima to media, the infiltration of inflammatory cells, the expression of inflammatory cytokines (NF‐κB, IL‐1β, IL‐6, TNF‐α, MCP‐1), adhesion molecules (ICAM‐1, VCAM‐1), and eNOS were measured. The results showed that cigarette smoke exposure aggravated the stenosis of the lumen, promoted the infiltration of inflammatory cells and induced the expression of the inflammatory cytokines and adhesion molecules after the balloon‐induced carotid artery injury. Moreover, cigarette smoke exposure can inhibit the expression of eNOS. Particularly, we surprised that melatonin could minimize this effect caused by cigarette smoke. These results suggested that melatonin could prevent the cigarette smoke‐induced restenosis in rat carotid arteries after balloon injury and the mechanism of its protective effect may be the inhibition of the inflammatory reaction. This also implies melatonin has the potential therapeutic applicability in prevention of restenosis after the vascular angioplasty in smokers.     

Automation of the in vitro micronucleus and chromosome aberration assay for the assessment of the genotoxicity of the particulate and gas–vapor phase of cigarette smoke

Abstract

Total particulate matter (TPM) and the gas–vapor phase (GVP) of mainstream smoke from the Reference Cigarette 3R4F were assayed in the cytokinesis-block in vitro micronucleus (MN) assay and the in vitro chromosome aberration (CA) assay, both using V79-4 Chinese hamster lung fibroblasts exposed for up to 24?h. The Metafer image analysis platform was adapted resulting in a fully automated evaluation system of the MN assay for the detection, identification and reporting of cells with micronuclei together with the determination of the cytokinesis-block proliferation index (CBPI) to quantify the treatment-related cytotoxicity. In the CA assay, the same platform was used to identify, map and retrieve metaphases for a subsequent CA evaluation by a trained evaluator. In both the assays, TPM and GVP provoked a significant genotoxic effect: up to 6-fold more micronucleated target cells than in the negative control and up to 10-fold increases in aberrant metaphases. Data variability was lower in the automated version of the MN assay than in the non-automated. It can be estimated that two test substances that differ in their genotoxicity by approximately 30% can statistically be distinguished in the automated MN and CA assays. Time savings, based on man hours, due to the automation were approximately 70% in the MN and 25% in the CA assays. The turn-around time of the evaluation phase could be shortened by 35 and 50%, respectively. Although only cigarette smoke-derived test material has been applied, the technical improvements should be of value for other test substances.     

Household Smoking and Childhood Asthma in the United States: A State-Level Analysis

Background. The reason for the substantial geographic variation in the prevalence of childhood asthma is not known. Objective. To investigate the association between exposure to cigarette smoking in the home and childhood asthma at the state-level, toward improving current understanding of geographic variation in childhood asthma rates. Methods. Data were drawn from the National Children's Health Survey (NCHS, 2003), a representative sample (n = 102, 000) of youth 0 to 17 years of age in the United States. Household smoking and asthma in children were reported by parents. Air quality for each state was obtained from Environmental Protection Act (EPA) reports, and state-level poverty reports were obtained from the US Department of Agriculture. Results. Household smoking was associated with a statistically significant increase in risk of asthma among children at the state level (p = 0.026). This association did not appear to be influenced by outdoor air quality at the state level or socioeconomic position. Conclusions. These results are the first to show a link between cigarette smoking in the home and childhood asthma at a state-level in the United States.     

Low-level environmental tobacco smoke exposure and inflammatory biomarkers in children with asthma

Objective: The effects of low-level environmental tobacco smoke (ETS) exposure, on asthma control, lung function and inflammatory biomarkers in children with asthma have not been well studied. The objective of the study was to assess ETS exposure in school-age children with asthma whose parents either deny smoking or only smoke outside the home, and to assess the impact of low-level ETS exposure on asthma control, spirometry and inflammatory biomarkers. Methods: Forty patients age 8–18 years with well-controlled, mild-to-moderate persistent asthma treated with either inhaled corticosteroids (ICS) or montelukast were enrolled. Subjects completed an age-appropriate Asthma Control Test and a smoke exposure questionnaire, and exhaled nitric oxide (FeNO), spirometry, urinary cotinine and leukotriene E₄ (LTE₄) were measured. ETS-exposed and unexposed groups were compared. Results: Only one parent reported smoking in the home, yet 28 (70%) subjects had urinary cotinine levels ≥1?ng/ml, suggesting ETS exposure. Seven subjects (18%) had FeNO levels >25parts per billion, six of whom were in the ETS-exposed group. In the ICS-treated subjects, but not in the montelukast-treated subjects, ETS exposure was associated with higher urinary LTE₄, p?=?0.04, but had no effect on asthma control, forced expiratory volume in 1?s or FeNO. Conclusions: A majority of school-age children with persistent asthma may be exposed to ETS, as measured by urinary cotinine, even if their parents insist they don’t smoke in the home. Urinary LTE₄ was higher in the ETS-exposed children treated with ICS, but not in children treated with montelukast.