Ruth A. Etzel

Measuring the exposure of infants to tobacco smoke. Nicotine and cotinine in urine and saliva.

The effect of parental smoking on the well-being of infants and children is an important public health concern. It is necessary, however, to validate the existence of such exposure objectively before an evaluation of the effects of parental smoking behavior on the childs health can be made. We measured the concentration of nicotine and its major metabolite, cotinine, in the saliva and urine of 32 infants with household exposure to tobacco smoke, and 19 unexposed infants. The concentrations were significantly higher in the exposed group than in the unexposed group, with the best indicator of chronic exposure being the urinary cotinine:creatinine ratio; median in the exposed group, 351 ng per milligram (225.3 nmol per millimole); median in the unexposed group, 4 ng per milligram (2.6 nmol per millimole) (P less than 0.0001). There was a direct relation between cotinine excretion by the infants and the self-reported smoking behavior of the mothers during the previous 24 hours (r = 0.67, P = 0.0001). Our results indicate that infants who were exposed to tobacco smoke absorbed its constituents and that urinary excretion of cotinine is a reliable measure of such exposure in infants.

A review of the use of saliva cotinine as a marker of tobacco smoke exposure

Cotinine, the major metabolite of nicotine, is a useful marker of exposure to tobacco smoke. It can be measured in plasma, urine, or saliva. However, distinguishing between active and passive smoking on the basis of a cotinine measurement may be difficult. In order to evaluate the relationship between saliva cotinine concentration and self-reported tobacco smoke exposure in both active and passive smokers, an English-language literature search using MEDLINE was conducted (1973-1989), and the bibliographies of identified articles were reviewed. Of 43 originally identified articles, only 22 met the criteria for inclusion. Specific information regarding population studied, reported tobacco smoke exposure, method of measurement, and cotinine concentrations was assessed. Passive smokers usually have cotinine concentrations in saliva below 5 ng/ml, but heavy passive exposure can result in levels greater than or equal to 10 ng/ml. Levels between 10 and 100 ng/ml may result from infrequent active smoking or regular active smoking with low nicotine intake. Levels greater than 100 ng/ml are probably the result of regular active smoking. Four categorizations of tobacco smoke exposure are suggested on the basis of saliva cotinine concentrations.

Ultraviolet light: A hazard to children

BACKGROUND Sunlight is subdivided into visible light, ranging from 400 nm (violet) to 700 nm (red); longer infrared, “above red” or .700 nm, also called heat; and shorter ultraviolet radiation (UVR), “below violet” or ,400 nm. UVR is further subdivided into UV-A (320–400 nm), also called black (invisible) light; UV-B (290–320 nm), which is more skin-penetrating; and UV-C (,290 nm). UV-B constitutes ,0.5% of sunlight reaching the earth’s surface, but is responsible for most of the acute and chronic sunrelated damage to normal skin.1 Most UVR is absorbed by stratospheric ozone. UV-B has greater intensity in summer than in winter, at midday than in morning or late afternoon, in places closer to the equator, and at high altitudes. Sand, snow, concrete, and water can reflect up to 85% of sunlight, thus intensifying exposure.1

Policy statement - Tobacco use: A pediatric disease

Tobacco use and secondhand tobacco-smoke (SHS) exposure are major national and international health concerns. Pediatricians and other clinicians who care for children are uniquely positioned to assist patients and families with tobacco-use prevention and treatment. Understanding the nature and extent of tobacco use and SHS exposure is an essential first step toward the goal of eliminating tobacco use and its consequences in the pediatric population. The next steps include counseling patients and family members to avoid SHS exposures or cease tobacco use; advocacy for policies that protect children from SHS exposure; and elimination of tobacco use in the media, public places, and homes. Three overarching principles of this policy can be identified: (1) there is no safe way to use tobacco; (2) there is no safe level or duration of exposure to SHS; and (3) the financial and political power of individuals, organizations, and government should be used to support tobacco control. Pediatricians are advised not to smoke or use tobacco; to make their homes, cars, and workplaces tobacco free; to consider tobacco control when making personal and professional decisions; to support and advocate for comprehensive tobacco control; and to advise parents and patients not to start using tobacco or to quit if they are already using tobacco. Prohibiting both tobacco advertising and the use of tobacco products in the media is recommended. Recommendations for eliminating SHS exposure and reducing tobacco use include attaining universal (1) smoke-free home, car, school, work, and play environments, both inside and outside, (2) treatment of tobacco use and dependence through employer, insurance, state, and federal supports, (3) implementation and enforcement of evidence-based tobacco-control measures in local, state, national, and international jurisdictions, and (4) financial and systems support for training in and research of effective ways to prevent and treat tobacco use and SHS exposure. Pediatricians, their staff and colleagues, and the American Academy of Pediatrics have key responsibilities in tobacco control to promote the health of children, adolescents, and young adults.

Effects of Intermittent Ozone Exposure on Peak Expiratory Flow and Respiratory Symptoms among Asthmatic Children in Mexico City

In a panel study of Mexican children (5-13 y of age) with mild asthma, the authors studied the relationship between ozone exposure and the course of childhood asthma. Decrements in peak expiratory flow rate were associated with ozone, and respiratory symptoms were associated with both ozone level and ambient particulate matter (< 10 microm) level. After the authors adjusted for minimum temperature and autocorrelation in the data, they determined that an increase of 50 ppb in a daily ozone 1-h maximum was related to an 8% increase in cough (95% confidence interval = 2, 15); a 24% increase in phlegm (95% confidence interval = 13, 35); and an 11% increase in low respiratory symptoms index (95% confidence interval = 5, 19). The authors concluded that children with mild asthma who resided in the south of Mexico City were affected adversely by the high ozone ambient levels observed in this area.

Methyl Tertiary Butyl Ether in Human Blood after Exposure to Oxygenated Fuel in Fairbanks, Alaska

Residents of Fairbanks, Alaska reported health complaints when 15%, by volume, methyl tertiary butyl ether (MTBE) was added to gasoline during an oxygenated fuel program. We conducted an exposure survey to investigate the effect of the program on human exposure to MTBE. We studied 18 workers in December 1992 during the program and 28 workers in February 1993 after the program was suspended. All workers were heavily exposed to motor vehicle exhaust or gasoline fumes. In December, the median post-shift blood concentration of MTBE in the workers was 1.8 micrograms/l (range, 0.2-37.0 micrograms/l), and in February the median post-shift blood concentration of MTBE in the 28 workers was 0.24 micrograms/l (range, 0.05-1.44 micrograms/l; p = .0001). Blood MTBE levels were measurably higher during the oxygenated fuel program in Fairbanks than after the program was suspended.

Incidence of foodborne illnesses reported by the Foodborne Diseases Active Surveillance Network (FoodNet)-1997.

In 1997, the Foodborne Diseases Active Surveillance Program (FoodNet) conducted active surveillance for culture-confirmed cases of Campylobacter, Escherichia coli O157, Listeria, Salmonella, Shigella, Vibrio, Yersinia, Cyclospora, and Cryptosporidium in five Emerging Infections Program sites. FoodNet is a collaborative effort of the Centers for Disease Control and Preventions National Center for Infectious Diseases, the United States Department of Agricultures Food Safety and Inspection Service, the Food and Drug Administrations Center for Food Safety and Applied Nutrition, and state health departments in California, Connecticut, Georgia, Minnesota, and Oregon. The population under active surveillance for foodborne infections was approximately 16.1 million persons or roughly 6% of the United States Population. Through weekly or monthly contact with all clinical laboratories in these sites, 8,576 total isolations were recorded: 2,205 cases of salmonellosis, 1,273 cases of shigellosis, 468 cases of cryptosporidiosis, 340 of E. coli O157:H7 infections, 139 of yersiniosis, 77 of listeriosis, 51 of Vibrio infections, and 49 of cyclosporiasis. Results from 1997 demonstrate that while there are regional and seasonal differences in reported incidence rates of certain bacterial and parasitic diseases, and that some pathogens showed a change in incidence from 1996, the overall incidence of illness caused by pathogens under surveillance was stable. More data over more years are needed to assess if observed variations in incidence reflect yearly fluctuations or true changes in the burden of foodborne illness.

Environmental tobacco smoke exposure and health effects in children: results from the 1991 National Health Interview Survey.

OBJECTIVE: To determine the effect of environmental tobacco smoke exposure on the health of children in the United States. DESIGN AND SETTING: Cross-sectional study of children who participated in the 1991 National Health Interview Survey. PARTICIPANTS: 17448 children residing in the United States. MAIN OUTCOME MEASURES: Rates of respiratory illnesses and all illnesses, and the morbidity due to these illnesses, in children exposed to environmental tobacco smoke in the home daily compared with those in children not exposed in the home. Our analyses controlled for age, socioeconomic status, race, family size, sex, season, and region of the country. RESULTS: Children who were exposed to environmental tobacco smoke had a higher incidence of acute respiratory illnesses (relative risk (RR) = 1.10, 95% confidence interval (CI) 0.95 to 1.26) and all chronic respiratory diseases (RR = 1.28, 95% CI 0.99 to 1.65) than children who were not exposed, although both CIs included unity, and chance cannot be ruled out as being responsible for these findings. Children who were exposed to environmental tobacco smoke had, on average, 1.87 more days of restricted activity (95% CI 0.20 to 3.54), 1.06 more days of bed confinement (95% CI 0.20 to 1.92), and 1.45 more days of school absence (95% CI 0.40 to 2.50) per year than children who were not exposed. CONCLUSIONS: Environmental tobacco smoke exposure in the home, which is completely preventable, is an important predictor of increased morbidity in children.

Impact of ambient temperature on children's health: A systematic review

Children are vulnerable to temperature extremes. This paper aimed to review the literature regarding the relationship between ambient temperature and childrens health and to propose future research directions. A literature search was conducted in February 2012 using the databases including PubMed, ProQuest, ScienceDirect, Scopus and Web of Science. Empirical studies regarding the impact of ambient temperature on childrens mortality and morbidity were included. The existing literature indicates that very young children, especially children under one year of age, are particularly vulnerable to heat-related deaths. Hot and cold temperatures mainly affect cases of infectious diseases among children, including gastrointestinal diseases, malaria, hand, foot and mouse disease, and respiratory diseases. Pediatric allergic diseases, like eczema, are also sensitive to temperature extremes. During heat waves, the incidences of renal disease, fever and electrolyte imbalance among children increase significantly. Future research is needed to examine the balance between hot- and cold-temperature related mortality and morbidity among children; evaluate the impacts of cold spells on cause-specific mortality in children; identify the most sensitive temperature exposure and health outcomes to quantify the impact of temperature extremes on children; elucidate the possible modifiers of the temperature and childrens health relationship; and project childrens disease burden under different climate change scenarios.

Early-life prevention of non-communicable diseases

Non-communicable diseases (NCDs) are major causes of death worldwide and underlie almost two-thirds of all global deaths.1 Although all countries face epidemics of these diseases, low-income and middle-income countries, and the poorest and most vulnerable populations within them, are affected the most. There is a global imperative to create and implement effective prevention strategies, because the future costs of diagnosis and treatment are likely to be unaffordable. At the UN High-Level Meeting on the Prevention and Control of Non-Communicable Diseases, held in New York, USA, in September, 2011, the so-called four by four strategy for NCD prevention was proposed. Prevention efforts for the priority NCDs discussed at the meeting (diabetes, cardiovascular disease, cancer, and chronic obstructive pulmonary disease) focus on four, mainly adult, risk factors: poor diet, physical inactivity, tobacco use, and alcohol consumption. Although paragraphs 26 and 28 of the UN Political Declaration refer to the roles of prenatal nutrition, maternal diseases, and household air pollution on NCD risk in later life, these paragraphs only partially describe the full scope of the problem and opportunities for intervention. As scientific knowledge emerges on the role of both nutritional factors and exposures to environmental chemicals in the developmental origins of health and disease, evidence suggests that much more attention is needed on early-life interventions, optimisation of nutrition, and reduction of toxic exposures to curtail the increasing prevalence of NCDs. The present state of the science on the developmental origins of health and disease and NCDs was discussed at the Prenatal Programming and Toxicity III conference, Environmental Stressors in the Developmental Origins of Disease: Evidence and Mechanisms, held in Paris, France in May, 2012, and at a symposium just before the conference.2 Studies in human beings have shown that nutritional deprivation and maternal metabolic status (eg, diabetes) in early intrauterine life increase the risk of metabolic disorders and cardiovascular disease in adulthood.3,4 These effects occur not only in settings of extreme deprivation, but also throughout the normal range of population weights at birth and in early childhood.3 Investigators have also reported associations between in-utero exposures and childhood diseases, including type 2 diabetes.5 In-utero and early-life exposures to environmental toxicants, ranging from heavy metals to endocrine-disrupting chemicals, affect adult metabolism, immune system function, neurodevelopment, and reproductive function.2 Although causal relations have not yet been established, the new science of epigenetics offers insight into mechanisms of early life predisposition to adult disease risk. During development, epigenetic marks, such as DNA methylation, histone modifications, and noncoding RNA expression, undergo substantial changes. These changes affect genes that are essential for both early life development and later life physiological functions. Epigenetic modifications are stable during cell division and can be transmitted transgenerationally.6 An increasing amount of evidence suggests that developmental exposure to nutritional imbalance or environmental contaminants—including metals, pesticides, persistent organic pollutants, and chemicals in drinking water, such as triethyltin, chloroform, and trihalomethanes—can affect epigenetic changes, thus suggesting a mechanism for their effects on adult health.7,8 Similarly, prenatal exposure to air pollutants has been associated with epigenetic changes and subsequent effects on children’s respiratory health.9 Knowledge that in-utero and early childhood experiences affect the risk of NCD development provides an opportunity to target interventions at the time when they have the greatest effect. Because these exposures are not controlled directly by the individual, especially when the exposures might have occurred to the individual’s parents or grandparents, early-life interventions can reduce the perception of blame that the individual’s own lifestyle has caused his or her disease. This notion has policy implications, because the prevailing viewpoint often assumes that NCDs are mainly a matter of individual responsibility, thus obviating societal and governmental responsibility. Substantial reductions of NCD risks could be achieved through the use of existing maternal–child health platforms to educate mothers about both nutritional and environmental exposures and to integrate the health promotion and disease prevention agendas within social and economic development efforts. For example, the Millennium Development Goals (MDGs) address not only maternal and child health problems, but also poverty and malnutrition, sex inequality, and lack of education, all of which are notable drivers of social disadvantage in low-income and middle-income countries and are underlying causes of NCDs.10,11 Poverty alleviation, sustainable food production, and reductions in exposures to toxic chemicals are all key themes emerging from the Rio+20 UN Conference on Sustainable Development12 held in Rio de Janeiro, Brazil, in June, 2012, and the development of Sustainable Development Goals (SDGs) and appropriate environmental, nutritional, and health indicators provides another opportunity to incorporate NCD prevention into broader, multisector programmes. The integration of NCD prevention with the attainment of the MDGs and SDGs could leverage major worldwide investments in health and development.