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Environmental Tobacco Smoke

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Overview :

Several of the Centers for Children's Environmental Health and Disease Prevention Research continue to study the effects of environmental tobacco smoke (ETS) on children.  ETS is sometimes also called secondhand smoke.

ETS is a complex mixture of gases and particulate matter, which contains over 4,500 compounds in both vapor and particle phases, including many toxic agents.  Constituents of ETS include carbon monoxide, nicotine, ammonia, acrolein, acetone, formaldehyde, respirable suspended particulates (RSPs), polycyclic aromatic hydrocarbons (PAHs), some of which are known animal carcinogens, and heavy metals, including cadmium and lead (Matt et al. 2004).  ETS is classified as a Class A human carcinogen by the U.S. EPA and is responsible for approximately 3,000 lung cancer deaths annually among U.S. non-smokers.  ETS contains a number of chemicals whose industrial emissions are regulated as hazardous air pollutants (HAPs).  A recent analysis identified six, acetaldehyde, acrolein, acrylonitrile benzene, 1,3 butadiene and formaldehyde, as contributing significantly to overall health risks from chronic residential ETS exposure (Nazaroff and Singer 2004).  Vapor phase components of ETS deposit and are adsorbed onto walls, furniture, clothing and toys within a short period after emission.  Vapor phase components are re-emitted into the air over the period of days to months.  Particulate matter can deposit on surfaces within hours after smoking and be re-suspended or react with vapor-phase components (Matt et al. 2004).

An estimated 40 percent of U.S. children are exposed to ETS at home.  The EPA concludes that passive smoking results in serious respiratory problems for infants and young children, estimating that exposure to ETS worsens the condition of 200,000 to 1 million asthmatic children each year (U.S. EPA 1993).  ETS exposure in children has been linked to middle ear disease and sudden infant death syndrome (SIDS).  Recent analysis of NHANES III data also shows an inverse association between ETS exposure and cognitive deficits in children 6-16 years of age (Yolton et al. 2005). 

Epidemiological and experimental data have established the adverse effects of numerous environmental toxicants, including lead, alcohol, mercury, PCBs, and ETS on children’s brain function.  In utero exposure to these toxicants has been linked with cognitive deficits and behavioral problems.  Lead exposure has been linked to specific behavioral problems, including conduct disorder and delinquency, mental retardation and ADHD-like behavior.  However, many studies linking environmental toxicants with neurobehavioral effects have only examined children with high exposures.  There is emerging evidence that adverse effects of exposure to lead, mercury, and PCBs occur at levels previously thought low.

Projects : Children's Center Research on ETS

Cincinnati Children’s Environmental Health Center

Researchers at the Cincinnati Children's Center have demonstrated a link between Environmental Tobacco Smoke (ETS) exposure and cognitive skills among children and adolescents.  They have also shown a link between exposure to both ETS and lead and the development of attention deficit/hyperactivity disorder (ADHD).  The Center has been examining meconium, or a baby’s first stools, as a way to measure the exposure a fetus received to environmental chemicals, including ETS, while in the womb.  Meconium is a repository of many xenobiotic substances that the fetus has been exposed to in utero starting from the 12th week of gestation until birth.  It has a number of benefits as a cumulative measure of fetal exposure. 

Researchers at the Cincinnati Children’s Center demonstrated a link between Environmental Tobacco Smoke (ETS) exposure and cognitive skills among children and adolescents.

The study examined data collected on nearly 4,400 US children and adolescents, aged 6-16, for the National Health and Nutrition Examination Survey – III (NHANES-III) during 1988-1994.  ETS exposure was estimated by measures of serum cotinine.  Cotinine is a product created when the body breaks down nicotine and is an excellent biomarker of exposure to ETS.  It can be measured in many bodily fluids and products.  For this study, cotinine was measured in blood serum.  Children were selected for inclusion in the study if they reported no use of tobacco products in the five days prior to testing.  If these participants had levels of serum cotinine, then that would indicate they were exposed to ETS even though they were not active smokers. 

Children were given tests of reading, math, reasoning, and memory.  Results showed that children who had higher levels of cotinine in their serum also scored lower on tests of reading, math, and reasoning.  These relationships remained even at extremely low levels of ETS exposure.  The study found that as little as one nanogram of cotinine per milliliter of blood appeared to reduce IQ scores by an average of two points.  Being around one parent smoking less than a pack a day could produce that cotinine level in a child.

The study found that about 25 percent of mothers either smoke continuously or are exposed to tobacco products in their home.  Forty-three percent of children in the U.S. are exposed to ETS in their own homes, and the researchers found that 85% of children show some level of exposure through their serum.  Estimates from the study are that reading skills for over 13 million children could be affected by ETS exposure.

The study found that even a very small exposure to ETS, such as being around a one parent smoking less than a pack a day, appeared to reduce IQ scores by an average of two points (Yolton et al 2005). 

Exposure to both ETS and lead has been implicated in the development of attention deficit/hyperactivity disorder (ADHD) in children. A team of investigators, including researchers from the Cincinnati Children’s Environmental Center, confirmed links between both neurotoxicants and development of ADHD (Braun et al. 2006).  The researchers analyzed data from more than 3,800 children 4-15 years of age participating in the National Health and Nutrition Examination Survey (NHANES).  They found that children exposed prenatally to ETS were 2.5 times more likely to develop ADHD than children who were not exposed.  Children with a blood lead concentration greater than two micrograms per deciliter were four times more likely to develop ADHD than children with the lowest blood lead concentrations.  The study found that one in three cases of ADHD could be attributed to either prenatal exposure to ETS or childhood lead exposure.  The researchers conclude that exposure to prenatal tobacco and environmental lead are risk factors for ADHD in U.S. children.

Parents who smoke should be careful to avoid exposing their children to ETS.  Parents who do not smoke should be aware of places where their children can become exposed to ETS and take steps to protect them.

The Cincinnati Children’s Center has demonstrated that meconium shows a high degree of promise as a cumulative measure of fetal exposure, as well as a more direct measure of what gets into the fetal compartment. 

The presence of cotinine, the primary metabolite of nicotine, is used as a biomarker.  One of the principal advantages of obtaining biomarker measurements is that they represent the integrated dose from combined exposures and may more accurately reflect dose than other measurements (Bradman and Whyatt 2005).  However, because many of them, including nicotine and cotinine in most body fluids, have a short half-life in the body, they generally provide only transient dosimeters, providing the need for repeated samples.  Establishing an optimal matrix of biomarkers for ETS will need to take into account absorption, distribution, metabolism and excretion of its measurable components, and multiple samples may be needed due to the variability of environmental chemicals in biological samples (Lanphear and Bearer 2005).

Infants whose meconium contained more metabolites than that found in meconium of infants from abstaining women performed more poorly on the Bayley Scales of Infant Development.  Cincinnati researchers have proposed that environmental toxicants as well as nicotine and ethanol metabolites in meconium are useful biological markers for exposure to developmental neurotoxicants and may indicate infants at risk for poor neurodevelopment. 

Some of the advantages to using meconium as a way to measure ETS exposure to the developing fetus are that it is non-invasive, is metabolically inert, fetal tissue is deposited in the meconium after the first trimester, usually without any loss before birth, making it useful for assessment of long-term prenatal exposure to tobacco products, and so provides a direct measure of what enters the fetal compartment.

Meconium measures correlate well with reported maternal exposure to tobacco, and meconium cotinine levels are directly proportional to maternal report of the number of cigarettes smoked each day during pregnancy.

There are some disadvantages, however, which include that there is not any information from the first trimester, standards are still in development to quantify measurements made with meconium, and there is not a definitive way to relate these to measurements in more commonly used method other biological media such as urine, blood and saliva.

A current project is testing how various biomarkers, including hair, blood serum and urine, compare with maternal report of ETS exposure, PCB and DDT levels. 

Columbia Center for Children’s Environmental Health

This community-based participatory research (CBPR) project is examining how prenatal exposure to air pollution, environmental tobacco smoke (ETS) and pesticides may adversely affect fetal growth, increase the risk of neurocognitive delay, and impair children's learning ability as they enter school.  Researchers have found that ETS in combination with exposure to urban air pollution, including polycyclic aromatic hydrocarbons (PAHs), can lead to reduced growth and development.

The overall aim of this project is to identify risks of childhood asthma from prenatal and postnatal exposure to urban pollutants, including PAHs, ETS and allergens.  A goal of the study is to characterize the roles played by environmental exposures in the development of atopy (allergy), persistent wheezing, asthma and/or increased asthma symptoms.  Another goal is to determine interactions between environmental exposures and susceptibility factors, before birth and through ages 5-7, to the development of atopy and adverse respiratory outcomes.  The research is documenting the biological triggers set in motion by environmental exposures as early as in utero that lead to asthma when children reach five through seven years of age.

Johns Hopkins Center for the Asthmatic Child in the Urban Environment

The results of the initial intervention study (Eggleston et al. 2005; Breysse et al. 2005) show that two percent of the PM10 values and seventeen percent of the PM2.5 values exceeded the EPA’s proposed National Ambient Air Quality Standards (NAAQS). The most important indoor contributor to these high levels of indoor particulate matter was environmental tobacco smoke (ETS).  It was determined that each cigarette smoked contributed approximately 1 ug/m3 of airborne particulate matter.  Overall, the results suggest that almost half of indoor air particulates in homes of persons smoking cigarettes can be attributed to cigarette smoke. The intervention was successful at reducing allergen and particulate matter levels but did not produce a marked improvement in allergy symptoms. This may be due to the fact that the asthma severity in the recruited participants was low.

The current intervention study is looking to see whether getting smokers in the home to stop smoking and an intervention with HEPA air filters can make a difference in terms of the severity of children’s asthma symptoms.

USC/UCLA Children’s Environmental Health Center

Projects

The purpose of this study was to investigate the ability of ETS to alter allergic responses. The hallmark of allergy and childhood asthma is the formation of allergic antibodies called immunoglobulin E (IgE) which react to foreign allergy materials (such as pollen).  The severity of allergic symptoms is determined by the amount of histamine released from cells. IgE and histamine levels were measured in the nasal secretions of young adults with allergies (ragweed) before and after experimental exposure to either environmental tobacco smoke or clean air in an environmentally controlled chamber. After exposure, subjects were challenged with either ragweed allergen or a placebo.

Four days after exposure to ETS/ragweed, the IGE levels were nearly 17 times higher than after the clean air/ragweed challenge.  Histamine levels were similarly increased. The authors concluded that these studies provide the first experimental evidence that secondhand smoke can exacerbate allergic responses in people with allergies, a demonstration with important public health implications. (Diaz-Sanchez et al. 2006).

Selected Results :

Related Research :

Children's Center Projects related to this topic
NCER Research Projects related to this topic

EPA provides a number of ways to learn about ETS/secondhand smoke.  For more information, please visit
http://www.epa.gov/iaq/asthma/shs.html

Smoke-free homes program
http://www.epa.gov/iaq/ets/

References :

Berkowitz GS, Wetmur JG, Birman-Deych E, Obel J, Lapinski RH, Godbold JH, Holzman IR, Wolff MS 2004. In utero pesticide exposure, maternal paraoxonase activity, and head circumference. Environ Health Perspect 112:388-391.

Bradman A, Whyatt RM 2005. Characterizing exposures to non persistent pesticides during pregnancy and early childhood in the National Children's Study: a review of monitoring and measurement methodologies. Environ Health Perspect 113:1092-1099.

Braun JM, Kahn RS, Froehlich T, Auinger P, Lanphear BP 2006. Exposures to Environmental Toxicants and Attention Deficit Hyperactivity Disorder in U.S. Children. Environ Health Perspect 114:1904-1909.

Breysse PN, Buckley TJ, Williams D, Beck CM, Jo SJ, Merriman B, Kanchanaraksa S, Swartz LJ, Callahan KA, Butz AM, Rand CS, Diette GB, Krishnan JA, Moseley AM, Curtin-Brosnan J, Durkin NB, Eggleston PA 2005.  Indoor exposures to air pollutants and allergens in the homes of asthmatic children in inner-city Baltimore.  Environ Res. 2005 Jun;98(2):167-76.

Diaz-Sanchez D, Rumold R, Gong, Jr. H.  2006.  Challenge with environmental tobacco smoke exacerbates allergic airway disease in human beings.  J Allergy Clin Immunol.  441-446.

Eggleston PA, Butz A, Rand C, Curtin-Brosnan J, Kanchanaraksa S, Swartz L, Breysse P, Buckley T, Diette G, Merriman B, Krishnan JA 2005.  Home environmental intervention in inner-city asthma: a randomized controlled clinical trial. Ann Allergy Asthma Immunol. 2005 Dec;95(6):518-24. Comment in:Ann Allergy Asthma Immunol. 2005 Dec;95(6):496-7.

Eskenazi B, Harley K, Bradman A, Weltzien E, Jewell NP, Barr DB, Furlong CE, Holland NT 2004. Association of in utero organophosphate pesticide exposure and fetal growth and length of gestation in an agricultural population. Environ Health Perspect 112:1116-1124.

Gilliland FD, Li YF, Saxon A, Diaz-Sanchez D 2004. Effect of glutathione-S-transferase M1 and P1 genotypes on xenobiotic enhancement of allergic responses: randomised, placebo-controlled crossover study. Lancet 363(9403):119-25.

Gilliland FD, Berhane K, Li YF, Rappaport EB, Peters JM 2003. Effects of early onset asthma and in utero exposure to maternal smoking on childhood lung function. Am J Respir Crit Care Med 167:917-924.

Gilliland FD, Li YF, Dubeau L, Berhane K, Avol E, McConnell R, Gauderman WJ, Peters JM 2002. Effects of glutathione S-transferase M1, maternal smoking during pregnancy, and environmental tobacco smoke on asthma and wheezing in children. Am J Respir Crit Care Med 166:457-463.

Lanphear BP, Bearer CF 2005. Biomarkers in paediatric research and practice. Arch Dis Child 90:594-600.

Li YF, Langholz B, Salam MT, Gilliland FD 2005. Maternal and grandmaternal smoking patterns are associated with early childhood asthma. Chest 127(4):1232-41.

Matt GE, Quintana PJ, Hovell MF, Bernert JT, Song S, Novianti N, Juarez T, Floro J, Gehrman C, Garcia M, Larson S 2004. Households contaminated by environmental tobacco smoke: sources of infant exposures. Tob Control 13:29-37.

Nazaroff WW, Singer BC 2004. Inhalation of hazardous air pollutants from environmental tobacco smoke in US residences. J Expo Anal Environ Epidemiol 14 Suppl 1:S71-S77.

Perera FP, Rauh V, Whyatt RM, Tsai WY, Bernert JT, Tu YH, Andrews H, Ramirez J, Qu L, Tang D 2004. Molecular evidence of an interaction between prenatal environmental exposures and birth outcomes in a multiethnic population. Environ Health Perspect 112:626-630.

Rauh VA, Whyatt RM, Garfinkel R, Andrews H, Hoepner L, Reyes A, Diaz D, Camann D, Perera FP 2004. Developmental effects of exposure to environmental tobacco smoke and material hardship among inner-city children. Neurotoxicol Teratol 26:373-385.

U.S. Environmental Protection Agency 1993.  Respiratory Health Effects of Passive Smoking: Lung Cancer and Other Disorders..  Washington, D.C.: Office of Health and Environmental Assessment. 1-7-1993.

Yolton K, Dietrich K, Auinger P, Lanphear BP, Hornung R 2005. Exposure to environmental tobacco smoke and cognitive abilities among U.S. children and adolescents. Environmental Health Perspective 113:98-103.

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