Postnatal Environmental Tobacco Smoke Research Articles

Environmental tobacco smoke and sudden infant death syndrome: a review

Environmental tobacco smoke (ETS), containing the developmental neurotoxicant, nicotine, is a prevalent component of indoor air pollution. Despite a strong association with active maternal smoking and sudden infant death syndrome (SIDS), information on the risk of SIDS due to prenatal and postnatal ETS exposure is relatively inconsistent. This literature review begins with a discussion and critique of existing epidemiologic data pertaining to ETS and SIDS. It then explores the biologic plausibility of this association, with comparison of the known association between active maternal smoking and SIDS, by examining metabolic and placental transfer issues associated with nicotine, and the biologic responses and mechanisms that may follow exposure to nicotine. Evidence indicates that prenatal and postnatal exposures to nicotine do occur from ETS exposure, but that the level of exposure is often substantially less than levels induced by active maternal smoking. Nicotine also has the capacity to concentrate in the fetus, regardless of exposure source. Experimental animal studies show that various doses of nicotine are capable of affecting a neonate's response to hypoxic conditions, a process thought to be related to SIDS outcomes. Mechanisms contributing to deficient hypoxia response include the ability of nicotine to act as a cholinergic stimulant through nicotinic acetylcholine receptor (nAChR) binding. The need for future research to investigate nicotine exposure and effects from non-maternal tobacco smoke sources in mid to late gestation is emphasized, along with a need to discourage smoking around both pregnant women and infants.

Perinatal environmental tobacco smoke exposure in rhesus monkeys: critical periods and regional selectivity for effects on brain cell development and lipid peroxidation.

Perinatal environmental tobacco smoke (ETS) exposure in humans elicits neurobehavioral deficits. We exposed rhesus monkeys to ETS during gestation and through 13 months postnatally, or postnatally only (6–13 months). At the conclusion of exposure, we examined cerebrocortical regions and the midbrain for cell damage markers and lipid peroxidation. For perinatal ETS, two archetypal patterns were seen in the various regions, one characterized by cell loss (reduced DNA concentration) and corresponding increases in cell size (increased protein/DNA ratio), and a second pattern suggesting replacement of larger neuronal cells with smaller and more numerous glia (increased DNA concentration, decreased protein/DNA ratio). The membrane/total protein ratio, a biomarker of neurite formation, also indicated potential damage to neuronal projections, accompanied by reactive sprouting. When ETS exposure was restricted to the postnatal period, the effects were similar in regional selectivity, direction, and magnitude. These patterns resemble the effects of prenatal nicotine exposure in rodent and primate models. Surprisingly, perinatal ETS exposure reduced the level of lipid peroxidation as assessed by the concentration of thiobarbituric acid reactive species, whereas postnatal ETS did not. The heart, a tissue that, like the brain, has high oxygen demand, displayed a similar but earlier decrease (2–3 months) in lipid peroxidation in the perinatal exposure model, whereas values were reduced at 13 months with the postnatal exposure paradigm. Our results provide a mechanistic connection between perinatal ETS exposure and neurobehavioral anomalies, reinforce the role of nicotine in these effects, and buttress the importance of restricting or eliminating ETS exposure in young children.

PRENATAL AMBIENT EXPOSURE TO POLYCYCLIC AROMATIC HYDROCARBONS IN AIR POLLUTION COMPOUNDS AND THE OCCURRENCE OF RESPIRATORY SYMPTOMS OVER THE FIRST YEAR OF LIFE

ISEE-100 Aim: The purpose of the study was to test the hypothesis that infants with higher levels of prenatal exposure to polycyclic aromatic hydrocarbons (PAHs) from fossil fuel combustion may be at greater risk of developing respiratory symptoms. Methods: The study was carried out in a cohort of 333 newborns in Krakow, Poland, followed over the first year of life, for whom the data from prenatal personal air monitoring of mothers in the second trimester of pregnancy were available. The relative risks of respiratory symptoms due to prenatal PAH exposure were adjusted for potential confounders (gender of child, birth weight, maternal atopy, maternal education as a proxy for the socio-economic status, exposure to postnatal environmental tobacco smoke, and moulds in households) in the Poisson regression models. Results: Increased risk related to prenatal PAH exposure was observed for the occurrence of various respiratory symptoms such as for barking cough (RR = 4.80; 95% CI = 2.73–8.44), wheezing without cold (RR = 3.83; 95% CI = 1.18–12.43), sore throat (RR = 2.56; 95% CI = 1.57–4.16), ear infection (RR = 1.82; 95% CI = 1.03–3.23), cough irrespective of respiratory infections (RR = 1.27; 95% CI = 1.07–1.52), and cough without cold (RR = 1.72; 95% CI = 1.02–2.92). PAH exposure had an impact on the duration of respiratory symptoms as well. Conclusion: Since barking cough and wheezing are basic features of allergic inflammation in bronchial airways, the results of the study suggest that prenatal PAH exposure may increase the risk of other factors that can enhance allergic reaction inflammation. PAH exposure may also increase respiratory symptoms in the postnatal period. The results indicate that reduction of prenatal exposure to these common urban pollutants can benefit respiratory health of infants. The study also calls attention to the fact that prenatal exposure to PAHs was not only related to higher occurrence of respiratory symptoms, but also inversely correlated with weight, length, and reduced head circumference at birth.

Prenatal Ambient Air Exposure to Polycyclic Aromatic Hydrocarbons and the Occurrence of Respiratory Symptoms over the First Year of Life

The purpose of the study was to test the hypothesis that infants with higher levels of prenatal exposure to polycyclic aromatic hydrocarbons (PAHs) from fossil fuel combustion may be at greater risk of developing respiratory symptoms. The study was carried out in a cohort of 333 newborns in Krakow, Poland, followed over the first year of life, for whom data from prenatal personal air monitoring of mothers in the second trimester of pregnancy were available. The relative risks of respiratory symptoms due to prenatal PAHs exposure were adjusted for potential confounders (gender of child, birth weight, maternal atopy, maternal education as a proxy for the socio-economic status, exposure to postnatal environmental tobacco smoke, and moulds in households) in the Poisson regression models. Increased risk related to prenatal PAH exposure was observed for various respiratory symptoms such as barking cough (RR = 4.80; 95% CI: 2.73-8.44), wheezing without cold (RR = 3.83; 95% CI: 1.18-12.43), sore throat (RR = 1.96; 95% CI: 1.38-2.78), ear infection (RR = 1.82; 95% CI: 1.03-3.23), cough irrespective of respiratory infections (RR=1.27; 95% CI: 1.07-1.52), and cough without cold (RR = 1.72; 95% CI: 1.02-2.92). The exposure to PAHs also had impact on the duration of respiratory symptoms. The effect of PAHs exposure on the occurrence of such symptoms as runny nose or cough was partly modified by the simultaneous exposure to postnatal passive smoking. The analysis performed for the duration of respiratory symptoms confirmed significant interaction between PAHs exposure and postnatal ETS for runny or stuffy nose (RR = 1.82; 95% CI: 1.57-2.10), cough (RR = 1.18; 95% CI: 0.99-1.40), difficulty in breathing (RR = 1.39; 95% CI: 1.01-1.92) and sore throat (RR = 1.74; 1.26-2.39). Obtained results support the hypothesis that prenatal exposure to immunotoxic PAHs may impair the immune function of the fetus and subsequently may be responsible for an increased susceptibility of newborns and young infants to respiratory infections.

Fetal and Postnatal Exposure to Tobacco Smoke and Respiratory Health in Children

The aim of this paper was to find out whether fetal exposure to environmental tobacco smoke (ETS), as compared to postnatal ETS exposure, is an independent risk factor for respiratory symptoms and diseases in younger schoolchildren. The cross-sectional epidemiological study comprised population of 1,561 Polish schoolchildren, aged 9-11 years. Information on the exposure to tobacco smoke and other sources of indoor air pollution at home, respiratory and allergic health status, and socio-economic status of the family was obtained by questionnaire survey. The respiratory health status was described by presence of wheezing, attacks of dyspnoea (noted during the last year or ever), bronchitis, wheezy bronchitis and asthma, ever diagnosed by a physician. Multivariate logistic regression analysis with adjustment for age, sex, area of residence, household density, damp and mould stains found at home, use of coal-fired stove, co-habitant pets, mother's education and paternal current and past smoking habit was used to assess the effect of fetal and postnatal exposures on respiratory health outcomes. The results of the multivariate analyses revealed statistically significant associations between fetal exposure to ETS and wheezing ever: log OR = 1.4 (95% CI: 1.0-2.0), attacks of dyspnoea ever: log OR = 1.8 (95% CI: 1.1-2.9), bronchitis: log OR = 2.1 (95% CI: 1.5-2.9), and wheezy bronchitis: log OR = 1.8 (95% CI: 1.1-2.9). The effect of postnatal ETS was statistically significant only for bronchitis: log OR = 1.4 (95% CI: 1.1-1.9). The results of our study showed that fetal exposure to tobacco smoke is an independent risk factor for symptoms of wheeze and wheezy bronchitis in schoolchildren when compared to postnatal ETS exposure.

Child Health and the Environment

In developed countries, people spend around 90% of their time indoors. Therefore, indoor air pollution could be a greater health hazard than outdoor air pollution. The possible components include tobacco smoke, the products of cooking, cleaning materials, insecticide sprays, and contaminants such as asbestos from work clothing. In the USA the Environmental Protection Agency has categorized indoor air pollution as one of the top five public health concerns. The subject receives close attention in Donald Wigle's Child Health and the Environment. Children are particularly vulnerable to indoor air pollutants because they inhale relatively high volumes of air per unit body weight and play on the floor where contaminant levels tend to be particularly high. The immaturity of organ systems and metabolic functions adds to the vulnerability of young children. Furthermore, children have little control over their own environment. The poor housing conditions of those from disadvantaged backgrounds may expose them to the pollutant hazards of dampness, degradation of building materials and lack of ventilation. Environmental tobacco smoke (ETS) is probably the best studied indoor air pollutant and represents an important preventable cause of childhood respiratory illness and death. Maternal exposure to ETS has been associated with increased risk of spontaneous abortion, preterm birth, low birthweight and intrauterine growth retardation. Childhood exposure to ETS has been associated with lung function deficits, exacerbation of asthma in preschool children and increased risk of lower respiratory tract infections. Also maternal and postnatal ETS exposure has been associated (weakly) with brain tumours, leukaemia and lymphomas. A meta-analysis of 39 studies of sudden infant death syndrome showed odds ratios of 2.1 (95% CI 1.8-2.4) for maternal smoking and 1.9 (1.6-2.4) for postnatal ETS. Carbon monoxide is another important indoor air pollutant to which children may be extra-susceptible on account of their high metabolic rates. The developing fetus is likewise at risk, not only because it has a higher oxygen demand but also because fetal haemoglobin has a high affinity for carbon monoxide. Volatile organic chemicals in the indoor environment include formaldehyde from chip-board, which can cause respiratory symptoms such as wheezing in children. Other such chemicals that may impact on child health include benzene from motor vehicles and paint solvents. In addition to chemicals, biological material from pets or house dust mites may be important. Pet allergens have been associated with asthma sensitization and house dust mites with asthma development. House dust mites and other allergens tend to be most concentrated on the floor, where children play. Child Health and the Environment, the first textbook of its kind, provides comprehensive coverage of current research areas. The early chapters give an overview of child environmental health, environmental epidemiology and risk assessment. The following nine chapters each address specific hazards including metals, polychlorinated biphenyls and dioxins, pesticides, hormonally active agents, radiation, indoor and outdoor air, and water. Each chapter is divided into health effects, exposures and risk management. The book does an excellent job at drawing together work from diverse areas and highlighting the many gaps in our knowledge.

Tobacco smoke exposure, wheeze, and atopy.

We investigated the effect of in utero and postnatal environmental tobacco smoke (ETS) exposure on respiratory symptoms and atopy in the first 3 years of life in children at high risk of allergic disease (both parents atopic). Three hundred and sixty-nine children were followed from birth and reviewed at ages 1 and 3 years (respiratory questionnaire, skin testing). Parental smoking questionnaires were administered, and plasma cotinine in cord and peripheral blood (at age 1 year) was measured (capillary column gas-liquid chromatography). Wheezing starting in the first year of life was significantly more common in children of smoking mothers (54.2% vs. 39.5%, P = 0.017), but not wheezing starting after age 1 year (10.8% vs. 10.9%, smoking and nonsmoking mothers, P = 0.99). Detectable cord cotinine was not associated with wheeze. More frequent wheeze in infancy was significantly more common in those with detectable 1-year cotinine (e.g., wheeze without colds, 17.8% vs. 5.6%, P = 0.02; wheeze most days, 6.5% vs. 0%, P = 0.04). ETS exposure was not associated with atopy. In the multivariate regression analysis, maternal smoking during pregnancy and/or in the first year of life remained associated with wheeze in the first year of life (odds ratio, 1.88; 95% confidence interval, 1.14-3.12; P = 0.01). ETS exposure in "high-risk" infants increases the risk of wheezing starting in the first year of life, but not after age 1 year. However, ETS exposure has little or no effect on the development of atopy. Measurement of plasma cotinine was no more useful than tobacco exposure assessment by questionnaire in our cohort.

Prenatal and Postnatal Environmental Tobacco Smoke Exposure and Children’s Health

Children's exposure to tobacco constituents during fetal development and via environmental tobacco smoke (ETS) exposure is perhaps the most ubiquitous and hazardous of children's environmental exposures. A large literature links both prenatal maternal smoking and children's ETS exposure to decreased lung growth and increased rates of respiratory tract infections, otitis media, and childhood asthma, with the severity of these problems increasing with increased exposure. Sudden infant death syndrome, behavioral problems, neurocognitive decrements, and increased rates of adolescent smoking also are associated with such exposures. Studies of each of these problems suggest independent effects of both pre- and postnatal exposure for each, with the respiratory risk associated with parental smoking seeming to be greatest during fetal development and the first several years of life.

Developmental effects of exposure to environmental tobacco smoke and material hardship among inner-city children

Because of the growing concern that exposures to airborne pollutants have adverse effects on fetal growth and early childhood neurodevelopment, and the knowledge that such exposures are more prevalent in disadvantaged populations, we assessed the joint impact of prenatal exposure to environmental tobacco smoke (ETS) and material hardship on the 2-year cognitive development of inner-city children, adjusted for other sociodemographic risks and chemical exposures. The purpose was to evaluate the neurotoxicant effects of ETS among children experiencing different degrees of socioeconomic disadvantage, within a minority population. The sample did not include children exposed to active maternal smoking in the prenatal period. Results showed significant adverse effects of prenatal residential ETS exposure and the level of material hardship on 2-year cognitive development, as well as a significant interaction between material hardship and ETS, such that children with both ETS exposure and material hardship exhibited the greatest cognitive deficit. In addition, children with prenatal ETS exposure were twice as likely to be classified as significantly delayed, as compared with nonexposed children. Postnatal ETS exposure in the first 2 years of life did not contribute independently to the risk of developmental delay, over and above the risk posed by prenatal ETS exposure. The study concluded that prenatal exposure to ETS in the home has a negative impact on 2-year cognitive development, and this effect is exacerbated under conditions of material hardship in this urban minority sample.

Lung C-fiber CNS reflex: role in the respiratory consequences of extended environmental tobacco smoke exposure in young guinea pigs.

Environmental tobacco smoke (ETS) exposure harms the respiratory health of children and is associated with an increased risk of asthma and sudden infant death syndrome (SIDS). The mechanisms by which ETS causes these effects are not understood. We hypothesized that one mechanism is an upregulation of the lung C-fiber central nervous system (CNS) reflex responses, which would result in exaggerated reflex responses of apnea, bronchoconstriction, and mucous hypersecretion. The purpose of this work is to highlight evidence obtained in an animal model of postnatal ETS exposure supporting the hypothesis and present data suggesting that actions of the neuropeptide substance P in the nucleus tractus solitarius (NTS) may contribute. Exposing young guinea pigs to sidestream smoke, the surrogate for ETS, for 5 weeks during the equivalent of human childhood, increased the excitability of afferent lung C fibers and NTS neurons in the CNS reflex pathway and prolonged the expiratory apnea. The findings suggest that an increased excitability of NTS neurons that can augment reflex output may contribute to respiratory symptoms in children exposed to ETS. Besides ETS exposure, substance P can also excite NTS neurons and augment lung C-fiber CNS reflex responses. Others have shown that substance P synthesis in lung C fibers is upregulated by another environmental stimulant, allergen. Thus, an upregulation of the substance P system at NTS synapses could contribute to the increased NTS excitability and enhanced reflex responses to lung C-fiber stimulation, providing a potential mechanism to help explain the association of ETS exposure with respiratory symptoms and SIDS.

Perinatal exposure to environmental tobacco smoke induces adenylyl cyclase and alters receptor-mediated cell signaling in brain and heart of neonatal rats

Perinatal exposure to environmental tobacco smoke (ETS) has adverse effects on neurobehavioral development. In the current study, rats were exposed to ETS during gestation, during the early neonatal period, or both. Brains and hearts were examined for alterations in adenylyl cyclase (AC) activity and for changes in β-adrenergic and m2-muscarinic cholinergic receptors and their linkage to AC. ETS exposure elicited induction of total AC activity as monitored with the direct enzymatic stimulant, forskolin. In the brain, the specific coupling of β-adrenergic receptors to AC was inhibited in the ETS groups, despite a normal complement of β-receptor binding sites. In the heart, ETS evoked a decrease in m2-receptor expression. In both tissues, the effects of postnatal ETS, mimicking passive smoking, were equivalent to (AC) or greater than (m2-receptors) those seen with prenatal ETS mimicking active smoking; the effects of combined prenatal and postnatal exposure were equivalent to those seen with postnatal exposure alone. These data indicate that ETS exposure evokes changes in cell signaling that recapitulate those caused by developmental nicotine treatment. Since alterations in AC signaling are known to affect cardiorespiratory function, the present results provide a mechanistic link reinforcing the participation of ETS exposure, including postnatal ETS, in disturbances culminating in events like Sudden Infant Death Syndrome.

Wheeze associated with prenatal tobacco smoke exposure: a prospective, longitudinal study

AIMSTo determine whether maternal smoking during pregnancy is a risk factor for reported wheeze in early childhood that is independent of postnatal environmental tobacco smoke (ETS) exposure and other known...

Association of prenatal maternal or postnatal child environmental tobacco smoke exposure and neurodevelopmental and behavioral problems in children.

We review the potential neurodevelopmental and behavioral effects of children's prenatal and/or postnatal exposure to environmental tobacco smoke (ETS). Children's exposure to ETS has been assessed in epidemiologic studies as a risk factor for a variety of behavioral and neurodevelopmental problems including reduced general intellectual ability, skills in language and auditory tasks, and academic achievement, and behavioral problems such as hyperactivity and decreased attention spans. We review 17 epidemiologic studies that have attempted to separate the effects of maternal active smoking during pregnancy from passive ETS smoke exposure by the pregnant mother or the child. Based on the available data, we found that ETS exposure could cause subtle changes in children's neurodevelopment and behavior. However, studies to date are difficult to interpret because of the unknown influence of uncontrolled confounding factors, imprecision in measurements of smoking exposure, and collinearity of pre- and postnatal maternal smoking. Although some evidence suggests that maternal smoking during pregnancy may be associated with deficits in intellectual ability and behavioral problems in children, the impact of prenatal or postnatal ETS exposure remains less clear.

Growth from birth to early adolescence in offspring prenatally exposed to cigarettes and marijuana.

Weight, height, and head circumference were examined in children from birth to early adolescence for whom prenatal exposure to marijuana and cigarettes had been ascertained. The subjects were from a low-risk, predominantly middle-class sample participating in an ongoing longitudinal study. The negative association between growth measures at birth and prenatal cigarette exposure was overcome, sooner in males than females, within the first few years, and by the age of six, the children of heavy smokers were heavier than control subjects. Pre and postnatal environmental tobacco smoke did not have a negative effect upon the growth parameters; however, the choice of bottle-feeding or shorter duration of breast-feeding by women who smoked during pregnancy appeared to play an important positive role in the catch-up observed among the infants of smokers. Prenatal exposure to marijuana was not significantly related to any growth measures at birth, although a smaller head circumference observed at all ages reached statistical significance among the early adolescents born to the heavy marijuana users.

Effect of pre‐ and postnatal tobacco smoke exposure on specific sensitization to food and inhalant allergens during the first 3 years of life

The study aimed to assess the effect of pre- and postnatal tobacco smoke exposure on specific sensitization to food allergens and inhalant allergens during the first 3 years of life. A total of 342 children of a prospective and observational birth cohort study on atopy (MAS) were included on the basis of a complete follow-up of specific IgE measurements at the ages of 1, 2, and 3 years with available questionnaire information about the parental smoking habit at birth, 18 months, and 3 years of age. Study children were grouped into four exposure categories representing in utero and postnatal environmental tobacco smoke (ETS) exposure, and according to the number of cigarettes smoked by the parents. The effect on the development of allergic sensitization to food, outdoor, and indoor allergens by 3 years of age was determined by multiple logistic regression analyses. At the age of 3, children who were pre- and postnatally exposed to tobacco smoke had a significantly higher risk of sensitization to food allergens (odds ratio: 2.3, 95% C.I.: 1.1-4.6) than unexposed children. Children who were only postnatally exposed by a smoking mother also had a 2.2 times higher risk (95% C.I.: 0.9-5.9) of sensitization than unexposed children. These two categories (pre- and/or postnatal exposure) contribute to the significant overall effect of the tobacco smoke exposure (P< or =0.02). No significant association between tobacco smoke exposure and specific sensitization to inhalant allergens was observed. The determining risk factors for this type of sensitization were atopic family history and mite- and cat-allergen exposure levels. During the first 3 years of life, both prenatal and postnatal tobacco smoke exposure has an adjuvant effect on allergic sensitization which seems to be restricted to allergens to which children are mainly exposed, in combination with the peak of the ETS exposure around the first birthday.