Do the medical history and physical examination predict low lung function?

BACKGROUND: We sought to determine whether an abnormal respiratory history or chest physical examination could be used to identify men with low lung function. METHODS: We analyzed pulmonary function, physical examination, and questionnaire data from 4461 middle-aged male Vietnam-era army veterans. MAIN RESULTS: The study sample consisted of 1161 never smokers, 1292 former smokers, and 2008 current smokers. Clinical indicators of respiratory disease (respiratory symptoms, respiratory signs, or a history of respiratory disease), were present in 26.1% of the never smokers, 31.7% of the former smokers, and 47.2% of the current smokers. We defined low forced expiratory volume in 1 second as a value less than 81.2% of the predicted value. Seven percent of the never smokers, 8% of the former smokers, and 17.3% of the current smokers demonstrated low forced expiratory volume in 1 second. Among those with a clinical indicator for spirometry only 11% of the never smokers, 13% of the former smokers, and 21% of the current smokers actually had a low forced expiratory volume in 1 second. Among those without a clinical indicator 6% of the never smokers, 6% of the former smokers, and 14% of the current smokers actually had a low forced expiratory volume in 1 second. CONCLUSIONS: The use of clinical indicators as a basis for obtaining pulmonary function tests in middle-aged men misses many with low lung function, especially current smokers.

Passive smoking and middle ear effusion among children in day care.

One hundred thirty-two children who attended a research day-care center were studied to determine whether passive tobacco smoke exposure was associated with an increased rate of otitis media with effusion or with an increased number of days with otitis media with effusion during the first 3 years of life. Based on preliminary studies, a serum cotinine concentration of greater than or equal to 2.5 ng/mL was considered indicative of exposure to tobacco smoke. Otitis media with effusion was diagnosed using pneumatic otoscopy by nurse practitioners and pediatricians who reviewed the children's health status each weekday. The 87 children with serum cotinine concentrations greater than or equal to 2.5 ng/mL had a 38% higher rate of new episodes of otitis media with effusion during the first 3 years of life than the 45 children with lower or undetectable serum cotinine concentrations (incidence density ratio = 1.38, 95% confidence interval 1.21 to 1.56). The average duration of an episode of otitis media with effusion was 28 days in the children with elevated cotinine concentrations and 19 days in the children with lower cotinine concentrations (P less than .01). It is estimated that 8% of the cases of otitis media with effusion in this population and 17.6% of the days with otitis media with effusion may be attributable to exposure to tobacco smoke.

Passive smoking alters lipid profiles in adolescents.

Although cigarette smoking is associated with elevation of plasma lipid levels and changes in lipoprotein distribution, it is not known whether passive smoking is associated with an alteration in lipid profiles. The relation between plasma cotinine, a marker of exposure to tobacco smoke, and lipid profiles was studied in healthy adolescents from a suburban New York high school district who were undergoing preparticipation sports physicals. Forty-four percent of the adolescents reported that one or both parents currently smoked. Eleven percent of the adolescents had plasma cotinine concentrations greater than or equal to 2.5 ng/mL, the level considered indicative of exposure. Adolescents with two smoking parents had significantly higher plasma cotinine concentrations after adjustment for other factors than adolescents whose parents did not smoke. Plasma cotinine concentration greater than or equal to 2.5 ng/mL was associated with an 8.9% greater ratio of total cholesterol to high-density lipoprotein cholesterol (P less than .003) and a 6.8% lower high-density lipoprotein cholesterol (P less than .03). These results suggest that passive smoking, like active smoking, leads to alterations in lipid profiles predictive of an increased risk of atherosclerosis.

Indoor air pollution and childhood asthma: effective environmental interventions.

Exposure to indoor air pollutants such as tobacco smoke and dust mites may exacerbate childhood asthma. Environmental interventions to reduce exposures to these pollutants can help prevent exacerbations of the disease. Among the most important interventions is the elimination of environmental tobacco smoke from the environments of children with asthma. However, the effectiveness of reducing asthmatic children's exposure to environmental tobacco smoke on the severity of their symptoms has not yet been systematically evaluated. Dust mite reduction is another helpful environmental intervention. This can be achieved by enclosing the child's mattresses, blankets, and pillows in zippered polyurethane-coated casings. Primary prevention of asthma is not as well understood. It is anticipated that efforts to reduce smoking during pregnancy could reduce the incidence of asthma in children. European studies have suggested that reducing exposure to food and house dust mite antigens during lactation and for the first 12 months of life diminishes the development of allergic disorders in infants with high total IgE in the cord blood and a family history of atopy. Many children with asthma and their families are not receiving adequate counseling about environmental interventions from health care providers or other sources.

Air pollution and bronchitic symptoms in Southern California children with asthma.

People who live in cities with dirty air have blacker lungs than people who live in rural areas with less air pollution. This is because, although particulates larger than 10 microm are filtered out when inhaled air passes through the nose, smaller particulates reach the lower airways. The particulates that reach the alveoli (the terminal air pockets of the lungs) stay there permanently. This accounts for the fact that a person who has lived in a polluted city for many years has blacker lungs than one who has lived in a polluted city for a shorter time.

Overview of investigations into pulmonary hemorrhage among infants in Cleveland, Ohio.

Idiopathic pulmonary hemorrhage was diagnosed in 37 infants in the Cleveland, Ohio, area between 1993 and 1998. This rare disorder has been related to 12 deaths, including 7 originally thought to be sudden infant death syndrome. Thirty of the infants were African American, all of whom lived in a limited geographic area of eastern metropolitan Cleveland, an area of older housing stock. An investigation led by the Centers for Disease Control and Prevention has found an association with household exposure to a toxigenic mold, Stachybotrys chartarum, and other fungi. The rapidly growing lungs of young infants appear to be especially vulnerable to the toxins made by toxigenic molds. Environmental tobacco smoke was frequently present in the infants' homes and may be a trigger precipitating the acute bleeding. Stachybotrys, although not thought to be a common mold, is known to have a wide geographic distribution. An additional 101 cases of acute, idiopathic pulmonary hemorrhage have been reported in infants in the United States over the past 5 years. In this overview, the investigations are summarized, the clinical profile is described, the toxicity of S. chartarum is discussed, and pathophysiologic concepts are presented.

Workshop to identify critical windows of exposure for children's health: immune and respiratory systems work group summary.

Fetuses, infants, and juveniles (preadults) should not be considered simply "small adults" when it comes to toxicological risk. We present specific examples of developmental toxicants that are more toxic to children than to adults, focusing on effects on the immune and respiratory systems. We describe differences in both the pharmacokinetics of the developing immune and respiratory systems as well as changes in target organ sensitivities to toxicants. Differential windows of vulnerability during development are identified in the context of available animal models. We provide specific approaches to directly investigate differential windows of vulnerability. These approaches are based on fundamental developmental biology and the existence of discrete developmental processes within the immune and respiratory systems. The processes are likely to influence differential developmental susceptibility to toxicants, resulting in lifelong toxicological changes. We also provide a template for comparative research. Finally, we discuss the application of these data to risk assessment.

Children's health and the environment: a new agenda for prevention research.

Patterns of illness in American children have changed dramatically in this century. The ancient infectious diseases have largely been controlled. The major diseases confronting children now are chronic and disabling conditions termed the "new pediatric morbidity"--asthma mortality has doubled; leukemia and brain cancer have increased in incidence; neurodevelopmental dysfunction is widespread; hypospadias incidence has doubled. Chemical toxicants in the environment as well as poverty, racism, and inequitable access to medical care are factors known and suspected to contribute to causation of these pediatric diseases. Children are at risk of exposure to over 15,000 high-production-volume synthetic chemicals, nearly all of them developed in the past 50 years. These chemicals are used widely in consumer products and are dispersed in the environment. More than half are untested for toxicity. Children appear uniquely vulnerable to chemical toxicants because of their disproportionately heavy exposures and their inherent biological susceptibility. To prevent disease of environmental origin in America's children, the Children's Environmental Health Network (CEHN) calls for a comprehensive, national, child-centered agenda. This agenda must recognize children's vulnerabilities to environmental toxicants. It must encompass a) a new prevention-oriented research focus; b) a new child-centered paradigm for health risk assessment and policy formulation; and c) a campaign to educate the public, health professionals, and policy makers that environmental disease is caused by preventable exposures and is therefore avoidable. To anchor the agenda, CEHN calls for long-term, stable investment and for creation of a national network of pediatric environmental health research and prevention centers.

Acute pulmonary hemorrhage in infants associated with exposure to Stachybotrys atra and other fungi.

BACKGROUND: A geographic cluster of 10 cases of pulmonary hemorrhage and hemosiderosis in infants occurred in Cleveland, Ohio, between January 1993 and December 1994. STUDY DESIGN: This community-based case-control study tested the hypothesis that the 10 infants with pulmonary hemorrhage and hemosiderosis were more likely to live in homes where Stachybotrys atra was present than were 30 age- and ZIP code-matched control infants. We investigated the infants' home environments using bioaerosol sampling methods, with specific attention to S atra. Air and surface samples were collected from the room where the infant was reported to have spent the most time. RESULTS: Mean colony counts for all fungi averaged 29 227 colony-forming units (CFU)/m3 in homes of patients and 707 CFU/m3 in homes of controls. The mean concentration of S atra in the air was 43 CFU/m3 in homes of patients and 4 CFU/m3 in homes of controls. Viable S atra was detected in filter cassette samples of the air in the homes of 5 of 9 patients and 4 of 27 controls. The matched odds ratio for a change of 10 units in the mean concentration of S atra in the air was 9.83 (95% confidence interval, 1.08-3 X 10(6)). The mean concentration of S atra on surfaces was 20 X 10(6) CFU/g and 0.007 x 10(6) CFU/g in homes of patients and controls, respectively. CONCLUSION: Infants with pulmonary hemorrhage and hemosiderosis were more likely than controls to live in homes with toxigenic S atra and other fungi in the indoor air.

Effect of increasing central venous pressure during passive heating on skin blood flow.

Whole body heating in humans increases skin blood flow (SkBF) and decreases central venous pressure (CVP). This study sought to identify whether elevations in SkBF are augmented during passive heating if CVP is increased during the heat stress. Seven subjects were exposed to passive heating. Once SkBF was substantially elevated, 15 ml/kg warm saline were rapidly infused intravenously. Whole body heating significantly increased cutaneous vascular conductance and decreased CVP from 7.7 +/- 0.6 to 4.9 +/- 0.5 mmHg (P < 0.05). Saline infusion returned CVP to pre-heat-stress pressures (7.9 +/- 0.6 mmHg; P > 0.05) and significantly increased cutaneous vascular conductance relative to the period before saline administration. Moreover, saline infusion did not alter mean arterial pressure, pulse pressure, or esophageal temperature (all P > 0.05). To serve as a volume control, 15 ml/kg saline were rapidly infused intravenously in normothermic subjects. Saline infusion increased CVP (P < 0.05) without affecting mean arterial pressure, pulse pressure, or cutaneous vascular conductance (all P > 0.05). These data suggest that cardiopulmonary baroreceptor unloading during passive heating may attenuate the elevation in SkBF in humans, whereas loading cardiopulmonary baroreceptors in normothermia has no effect on SkBF.

Lethal paralytic shellfish poisoning in Guatemala.

An outbreak of paralytic shellfish poisoning occurred in Champerico, on the Pacific coast of Guatemala, July-August 1987. Of 187 people affected with characteristic neurologic symptoms, 26 died. A case study implicated a species of clam, Amphichaena kindermani, harvested from local beaches as the vehicle of the neurotoxins (saxitoxins). Children less than 6 years old had a higher fatality rate (50%) than people greater than 18 years of age (7%). The minimum lethal dose for 1 child was estimated to have been 140 mouse units of toxin/kg body weight; thus children may be more sensitive to the saxitoxins than are adults. This is the first large outbreak of paralytic shellfish poisoning recognized in Guatemala.

Out-of-hospital deaths due to asthma in North Carolina, 1980-1988.

Because deaths that occur outside hospitals have not been well-described, we studied out-of-hospital deaths from asthma in North Carolina from 1980 through 1988. We investigated out-of-hospital deaths from asthma using information from the North Carolina Office of the Chief Medical Examiner. We excluded deaths for which a hospital was listed as the place where the death occurred. For the nine years studied, the Office of the Chief Medical Examiner recorded 89 of 158 investigated deaths from asthma as having occurred out of hospital. Of the 89 deaths, 73% occurred in the decedent's home. The rates of out-of-hospital deaths from asthma increased as the age of the decedents increased, were higher in rural countries than they were in urban counties, and were over three times higher for blacks and American Indians than they were for whites. Racial minorities may warrant special attention in any attempt to prevent out-of-hospital deaths due to asthma.

Restrictive workplace smoking policies: impact on nonsmokers' tobacco exposure.

The health consequences of exposure to environmental tobacco smoke (ETS) are well documented. Although nonsmokers are generally aware of the health risks of ETS exposure, the majority of nonsmokers are regularly exposed. The most common source of exposure is the workplace. Restrictive workplace smoking policies are being used as a primary means of reducing ETS exposure. However, few studies have focused on the relation between workplace policy and ETS exposure. We performed two studies which examined the relationship between smoking policy, self-reported ETS exposure, and salivary cotinine concentrations. Study I, a pilot study, focused on a workplace-based sample of 106 volunteers; Study 2 examined exposure among 881 nonsmokers in workplace settings. In both studies, more restrictive workplace smoking policies were associated with a lower proportion of nonsmoking volunteers with detectable salivary cotinine. In Study 2, the larger study, the only other variable found to be significantly related to cotinine detection was the presence of smokers in the home. These results suggest that restrictive workplace smoking policies may reduce employees' overall ETS exposure.

Indoor air pollutants in homes and schools.

Exposure to the four indoor air pollutants mentioned in this article may cause illnesses and fatalities in children. It is important for pediatricians to be aware of each of them and to remove children from environments contaminated with these pollutants. Guidance about monitoring the indoor air and interpreting the results is difficult to find. A chart of proposed guidelines may help the pediatrician faced with an indoor air problem (Table 1).

Asthma. The states' challenge.

At the national level, asthma is increasingly being recognized as an important public health problem. Because of the significant role of environmental exposure in asthma morbidity, public health agencies have a critical role to play in the surveillance and prevention of the disease. In April 1996, the Council of State and Territorial Epidemiologists, with assistance from the Centers for Disease Control and Prevention, surveyed state and territorial public health departments to determine the status of their asthma surveillance and intervention programs. Of the 51 health departments that responded, only eight reported that they had implemented an asthma control program within the previous 10 years. Reasons cited for not having programs included lack of funds, shortage of personnel, and asthma not being a priority. Most states were unable to assess the burden of asthma because they lack data or face barriers to using existing data. Removing barriers to the use of data is a first step toward defining the scope of the asthma problem.

Laboratory investigation of a poisoning epidemic in Sierra Leone.

In June 1986, an epidemic of poisoning occurred in Sierra Leone, West Africa; it involved 49 persons--with 14 deaths. Our laboratory's approach and investigation of this incident is described. Using positive chemical ionization mass spectrometry and nuclear magnetic resonance spectroscopy, the toxicant was identified as parathion, a highly toxic organophosphorus pesticide. Analysis of various items supported the epidemiologic hypothesis that bread was made from contaminated flour and that the flour became contaminated with parathion during a truck shipment. Modern analytical instruments played a major role in this laboratory investigation and effected the identification of the unknown toxicant within hours of receiving the initial bread sample. Close cooperation and clear communication between the epidemiologic and laboratory teams were important in this investigation.

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.

Use of a 24-hour recall diary to assess exposure to environmental tobacco smoke.

Methods to assess exposure to environmental tobacco smoke need to be valid and relatively easy to use. We therefore explored the use of a 24-h environmental tobacco smoke exposure-recall diary by comparing data from the 24-h diary with questionnaire responses and levels of salivary cotinine--a biochemical marker of environmental tobacco smoke exposure. A total of 875 nonsmokers at five Rhode Island worksites participated in the study. Twenty-five percent of the participants lived with smokers, and 96% had regular exposure to environmental tobacco smoke at work. Individuals who lived with smokers reported more exposures in the 24-h diary, both outside of work and during work hours, compared with those who had no smokers in their household. The correlation between saliva cotinine concentrations and the exposures recorded in the diary was weak (r = .10). Brief instruments for assessment of environmental tobacco smoke should be viewed cautiously, and use of this 24-h recall diary is not recommended.

Surveillance for dust storms and respiratory diseases in Washington State, 1991.

Southeast Washington State, which has a long history of seasonal dust storms, experienced 2 d of dust storms in October 1991, during which PM10 levels exceeded 1,000 micrograms/m3 (i.e., six times greater than the Environmental Protection Agency's 24-h PM10 standard). Three community hospitals in southeast Washington were visited for the purpose of assessing the possible effects of dust storms on respiratory health. During these visits, the number of emergency room visits for respiratory disorders for each day of 1991 were abstracted. These numbers were compared with daily PM10 levels for 1991. Also determined were the observed/expected ratios for the number of emergency room visits for each respiratory disorder category during October 1991. The maximum observed/expected ratio for the respiratory disorders was 1.2. For 1991, we found a 3.5% increase in the number of daily emergency room visits for bronchitis for each 100 micrograms/m3 increase in PM10. In addition, 2 d subsequent to those days on which the PM10 levels exceeded 150 micrograms/m3, there was a 4.5% increase in the number of emergency room visits for sinusitis for each 100 micrograms/m3 increase in PM10. Our results indicate that the naturally occurring PM10 in this setting has a small effect on the respiratory health of the population in general.

Active and passive smoking: hazards for children.

This manuscript describes the tobacco industry's efforts to recruit active smokers among the adolescent population, the effects of environmental tobacco smoke on nonsmokers, and lists some steps pediatricians can take to influence smoking behavior. Six health effects result from passive smoking. Children exposed to environmental tobacco smoke have increased lower respiratory illness rates, especially in the first year of life, passive smoking is associated with increased rates of chronic middle ear effusion in children. Exposure to cigarette smoke is associated with small changes in pulmonary function. Exposure to environmental tobacco smoke increases an asthmatic child's exacerbations. Exposure to environmental tobacco smoke is a risk factor for sudden infant death syndrome. Passive exposure during childhood to a parents smoking increases a child's risk of leukemia and lymphoma during adulthood. Pediatricians and others who care for children must try to limit as much as possible, the exposure of children to the cigarette smoke produced by others.