Occupational exposures and COPD: an ecological analysis of international data.

The occupational contribution to chronic obstructive pulmonary disease (COPD) has yet to be put in a global perspective. In the present study, an ecological approach to this question was used, analysing group-level data from 90 sex-specific strata from 45 sites of the Burden of Obstructive Lung Disease study, the Latin American Project for the Investigation of Obstructive Lung Disease and the European Community Respiratory Health Survey follow-up. These data were used to study the association between occupational exposures and COPD Global Initiative for Chronic Obstructive Lung Disease (GOLD) stage II or above. Regression analysis of the sex-specific group-level prevalence rates of COPD at each site against the prevalence of occupational exposure and ever-smoking was performed, taking into account mean smoking pack-yrs and mean age by site, sex, study cohort and sample size. For the entire data set, the prevalence of exposures predicted COPD prevalence (0.8% increase in COPD prevalence per 10% increase in exposure prevalence). By comparison, for every 10% increase in the proportion of the ever-smoking population, the prevalence of COPD GOLD stage II or above increased by 1.3%. Given the observed median population COPD prevalence of 3.4%, the model predicted that a 20% relative reduction in the disease burden (i.e. to a COPD prevalence of 2.7%) could be achieved by a 5.4% reduction in overall smoking rates or an 8.8% reduction in the prevalence of occupational exposures. When the data set was analysed by sex-specific site data, among males, the occupational effect was a 0.8% COPD prevalence increase per 10% change in exposure prevalence; among females, a 1.0% increase in COPD per 10% change in exposure prevalence was observed. Within the limitations of an ecological analysis, these findings support a worldwide association between dusty trades and chronic obstructive pulmonary disease for both females and males, placing this within the context of the dominant role of cigarette smoking in chronic obstructive pulmonary disease causation.

Relationship between lung function impairment and incidence or recurrence of cardiovascular events in a middle-aged cohort.

INTRODUCTION: Lung function impairment may be a risk factor for cardiovascular disease (CVD) events. OBJECTIVE: To determine the relationship between the severity of airflow obstruction based on modified Global Initiative on Obstructive Lung Disease (GOLD) criteria and the prevalence and incidence or recurrence of CVD in a cohort of US adults, aged 45-64 years, from 1987 to 2001. METHODS: We analysed data from 14 681 adults using logistic regression to determine the cross sectional association between lung function impairment and prevalent CVD at baseline and Cox regression to examine the prospective association of lung function impairment at baseline with CVD over 15 years of follow-up. Models were adjusted for age, sex, race, smoking, comorbid hypertension and diabetes, cholesterol levels and fibrinogen level. RESULTS: At baseline, the crude prevalence of CVD was higher among subjects with GOLD 2 (OR 2.9, 95% CI 2.4 to 3.6) and GOLD 3 or 4 chronic obstructive pulmonary disease (COPD) (OR 3.0, 95% CI 2.0 to 4.5), compared with normal subjects. These relative risks were greatly reduced after adjusting for covariates (OR 1.4, 95% CI 1.1 to 1.8 for GOLD 2 and OR 1.3, 95% CI 0.8 to 2.1 for GOLD 3 or 4). Similarly, the association between COPD and risk of incident or recurrent CVD was much stronger in the unadjusted models (hazard ratio (HR) 2.4, 95% CI 2.1 to 2.7 for GOLD 2 and 2.9, 95% CI 2.2 to 3.9 for GOLD 3 or 4) than in the adjusted ones (HR 1.2, 95% CI 1.03 to 1.4 for GOLD 2 and 1.5, 95% CI 1.1 to 2.0 for GOLD 3 or 4). CONCLUSION: We observed a crude association between lung function impairment and prevalent and incident or recurrent CVD that was greatly reduced after adjusting for covariates, including age, sex, race, smoking, comorbid hypertension and diabetes, cholesterol levels and fibrinogen level. These data suggest that this association may be, in part, mediated through established CVD risk factors included in our adjusted models.

Prevalence and outcomes of diabetes, hypertension and cardiovascular disease in COPD.

Chronic obstructive pulmonary disease (COPD) is associated with important chronic comorbid diseases, including cardiovascular disease, diabetes and hypertension. The present study analysed data from 20,296 subjects aged > or =45 yrs at baseline in the Atherosclerosis Risk in Communities Study (ARIC) and the Cardiovascular Health Study (CHS). The sample was stratified based on baseline lung function data, according to modified Global Initiative for Obstructive Lung Disease (GOLD) criteria. Comorbid disease at baseline and death and hospitalisations over a 5-yr follow-up were then searched for. Lung function impairment was found to be associated with more comorbid disease. In logistic regression models adjusting for age, sex, race, smoking, body mass index and education, subjects with GOLD stage 3 or 4 COPD had a higher prevalence of diabetes (odds ratio (OR) 1.5, 95% confidence interval (CI) 1.1-1.9), hypertension (OR 1.6, 95% CI 1.3-1.9) and cardiovascular disease (OR 2.4, 95% CI 1.9-3.0). Comorbid disease was associated with a higher risk of hospitalisation and mortality that was worse in people with impaired lung function. Lung function impairment is associated with a higher risk of comorbid disease, which contributes to a higher risk of adverse outcomes of mortality and hospitalisations.

Outdoor and indoor air pollution and COPD-related diseases in high- and low-income countries.

Chronic obstructive pulmonary disease (COPD) is an important cause of morbidity and mortality in both high- and low-income countries. While active cigarette smoking is the most important preventable risk factor globally, outdoor and indoor air pollutants can cause or exacerbate COPD. In high-income countries, historic air pollution events provide clear evidence that exposure to high levels of outdoor air pollutants is associated with increased mortality and morbidity due to COPD and related cardiorespiratory diseases. Studies in the last 20 years continue to show increased risk associated mainly with particulate matters, even at much lower levels. Populations in low-income countries are largely exposed to indoor air pollutants from the combustion of solid fuels, which contributes significantly to the burden of COPD-related diseases, particularly in non-smoking women. Effective preventive strategies for COPD may vary between countries, and include continued improvements in air cleaning technology, air quality legislation and dissemination of improved cooking stoves. A joint effort from both society and governments is needed for these endeavors.

Risk factors for prevalence of and mortality related to restriction on spirometry: findings from the First National Health and Nutrition Examination Survey and follow-up.

OBJECTIVE: To define risk factors for both restriction on spirometry and subsequent mortality in a national cohort of US adults. METHODS: Participants in the First National Health and Nutrition Examination Survey (NHANES I) were followed for up to 22 years. Subjects were classified using the forced expiratory volume in one second (FEV1), the forced vital capacity (FVC), and the FEV1/FVC ratio into subgroups with and without restriction on spirometry. Regression models were developed to determine risk factors for restriction on spirometry and death. RESULTS: Our final cohort consisted of 4320 subjects, of whom 481 (10.3 weighted %) had restriction on spirometry. The largest risk factors for restriction on spirometry were a cardiothoracic ratio of >55% (OR 4.3, 95%CI 3.1-5.9), race other than black or white (OR 3.7, 95%CI 1.8-7.8), and a history of stroke or paralysis (OR 1.8, 95%CI 1.1-2.9). The overall mortality rate was increased in subjects with restriction on spirometry (25.7 vs. 10.3 deaths per 1000 person-years). CONCLUSIONS: Restriction on spirometry is associated with comorbid disease and increased mortality, and is present in a significant proportion of the population.

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.

Obstructive lung disease and low lung function in adults in the United States: data from the National Health and Nutrition Examination Survey, 1988-1994.

BACKGROUND: Obstructive lung disease (OLD) is an important cause of morbidity and mortality in the US adult population. Potentially treatable mild cases of OLD often go undetected. This analysis determines the national estimates of reported OLD and low lung function in the US adult population. METHODS: We examined data from the Third National Health and Nutrition Examination Survey (NHANES III), a multistage probability representative sample of the US population. A total of 20,050 US adults participated in NHANES III from 1988 to 1994. Our main outcome measures were low lung function (a condition determined to be present if the forced expiratory volume in 1 second-forced vital capacity ratio was less than 0.7 and the forced expiratory volume in 1 second was less than 80% of the predicted value), a physician diagnosis of OLD (chronic bronchitis, asthma, or emphysema), and respiratory symptoms. RESULTS: Overall a mean (SE) of 6.8% (0.3%) of the population had low lung function, and 8.5% (0.3%) of the population reported OLD. Obstructive lung disease (age-adjusted to study population) was currently reported among 12.5% (0.7%) of current smokers, 9.4% (0.6%) of former smokers, 3.1% (1.1%) of pipe or cigar smokers, and 5.8% (0.4%) of never smokers. Surprisingly, 63.3% (0.2%) of the subjects with documented low lung function had no prior or current reported diagnosis of any OLD. CONCLUSIONS: This study demonstrates that OLD is present in a substantive number of US adults. In addition, many US adults have low lung function but no reported OLD diagnosis, which may indicate the presence of undiagnosed lung disease.

Sarcoidosis mortality in the United States 1979-1991: an analysis of multiple-cause mortality data.

PURPOSE: We sought to describe sarcoidosis mortality in the United States from 1979 through 1991. METHODS: We analyzed death certificate reports compiled by the National Center for Health Statistics for the period 1979 through 1991. RESULTS: Of the 26,866,600 people who died during the study period, 9,014 had a diagnosis of sarcoidosis listed on their death certificates. We restricted our study group to 5,791 people who died because of sarcoidosis or one of its complications. Among men, age-adjusted mortality rates increased from 1.3 per 1,000,000 in 1979 to 1.6 per 1,000,000 in 1991, and among women, these rates increased from 1.9 per 1,000,000 in 1979 to 2.5 per 1,000,000 in 1991. Age-adjusted mortality rates were consistently higher among blacks than whites. Age-adjusted mortality rates stratified by race, varied by state. Among whites, the highest rates were in northern states, while among blacks, the highest rates were in the Middle Atlantic and northern Midwestern states. CONCLUSIONS: Reported mortality due to sarcoidosis varies by region, sex, and race. We cannot determine whether these differences are related to characteristics of the disease, or problems in death certification and coding.

Risk factors for ARDS in the United States: analysis of the 1993 National Mortality Followback Study.

OBJECTIVE: To identify specific comorbid factors that are present in US decedents with ARDS. DESIGN: We searched the 1993 National Mortality Followback Study for all decedents who had a code for ARDS mentioned on their death certificate. We also searched for comorbid conditions both on the death certificates (sepsis, medical or surgical misadventures, cirrhosis) and in the study database (current or former smoking, use of alcohol at least 3 d/wk, race, gender, and age). We calculated proportional mortality ratios (PMRs) for these risk factors. RESULTS: Of the 19,003 decedents for whom data were available, 252 decedents, representing an estimated 19,460 US decedents, had ARDS listed on their death certificate. PMRs among decedents with ARDS were significantly increased for medical or surgical misadventures (PMR, 11.8; 95% confidence interval [CI], 3.8 to 36.7), sepsis (PMR, 5.6; 95% CI, 2.0 to 16.0), nonwhite race (PMR, 2.6; 95% CI, 1.4 to 5.0), and cirrhosis (PMR, 2.2; 95% CI, 1.1 to 4.6). PMRs were increased but not statistically significant for current smokers (PMR, 1.2; 95% CI, 0.5 to 3.0) or former smokers (PMR, 1.8; 95% CI, 0.7 to 4.3) compared to never smokers, and drinking alcohol on > or = 3 d/wk in the year prior to death, when compared to drinking alcohol less than < 3 d/wk (PMR, 1.8; 95% CI, 0.6 to 4.9). CONCLUSIONS: The results of this study confirm the positive associations between ARDS mortality and the presence of sepsis and cirrhosis, and suggest possible new relationships between ARDS mortality and nonwhite individuals and patients with medical or surgical misadventures.

Alpha 1-antitrypsin deficiency deaths in the United States from 1979-1991. An analysis using multiple-cause mortality data.

OBJECTIVE: To describe trends of reported alpha 1-antitrypsin deficiency mortality in the United States from 1979-1991. METHODS: We analyzed death certificate reports in the multiple-cause mortality files compiled by the National Center for Health Statistics. RESULTS: Of the 26,866,600 deaths that occurred during the 13-year period, 1,930 had alpha 1-antitrypsin deficiency listed as a cause of death. Over this period, we would have expected 5,400 to 13,400 persons with this condition to die. The age-adjusted mortality rate with reported alpha 1-antitrypsin deficiency listed increased 86%, from 4.3 per 10 million in 1979 to 8.0 per 10 million in 1991. alpha 1-Antitrypsin deficiency mortality rates were higher among whites than among blacks or persons of other races. alpha 1-Antitrypsin deficiency was listed in 2.7% of all deaths with obstructive lung disease among persons aged 35-44 years old and in 1.2% of all deaths listing hepatic disease among children aged 1 to 14 years old. CONCLUSIONS: alpha 1-Antitrypsin deficiency is an important risk factor for obstructive lung disease and hepatic disease in the United States, and it was reported with increasing frequency through the study period, although it is still likely underreported.

Predictors of cotinine levels in US children: data from the Third National Health and Nutrition Examination Survey.

STUDY OBJECTIVE: To determine what factors predict cotinine levels in US children. DESIGN: Cross-sectional study. SUBJECTS: Nationally representative sample of 5,653 US children, both with and without reported tobacco smoke exposure in their homes. METHODS: We stratified the children into those with reported passive smoke exposure at home and those without this exposure. We used regression models to predict the log of the cotinine level of the participants with the following independent covariates: age; race/ethnicity; number of rooms in the home; sex; parental education; family poverty index; family size; region; and, among children with reported passive smoke exposure, the number of cigarettes smoked in the home. RESULTS: Children exposed to passive smoke had a mean cotinine level of 1.66 ng/mL, and children not exposed to passive smoke had a mean level of 0.31 ng/mL. Among children with reported smoke exposure, non-Mexican-American race/ethnicity, young age, low number of rooms in the home, low parental education, and an increasing number of cigarettes smoked in the home were predictors of increased serum cotinine levels. Among children with no reported smoke exposure, significant predictors of increased cotinine levels included black race, young age, Midwest region of the United States, low number of rooms in the home, low parental education, large family size, and low family poverty index. CONCLUSION: While the reported number of cigarettes smoked in the home is the most important predictor of cotinine levels in children exposed to smoke and may provide an opportunity for clinical intervention, other demographic factors are important among children both with and without reported smoke exposure.

Lung cancer mortality rates in birth cohorts in the United States from 1960 to 1994.

We sought to describe the changing death rates from lung cancer in the US white population in sequential birth cohorts, adjusting for cohort smoking prevalence and duration. We searched the US mortality database (1960-1994) for all deaths among whites in which lung cancer was listed as the underlying cause of death. To determine the population at risk for lung cancer, we used the 1970, 1978-1980, and 1992 National Health Interview Surveys to estimate the annual number of current and recent smokers (those who had quit within 5 years) in 11 5-year birth cohorts, starting in 1901. We then determined annual lung cancer mortality rates for each birth cohort, stratified by sex and adjusting for the prevalence and duration of smoking. The population-based rates of lung cancer mortality were much higher among men than among women across all ages and birth cohorts, reflecting higher smoking rates among men. These differences decreased after we controlled for current and recent smoking within the cohorts and were slightly increased in women after we controlled for duration of smoking. Differences in lung cancer death rates across birth cohorts of US men and women primarily reflect differences in the prevalence and duration of smoking in these birth cohorts. Changes in cigarette design that have greatly reduced tar yields have a relatively small effect compared with that of people's smoking status and duration of smoking.

Cigarette smoking and thyroid hormone levels in males.

BACKGROUND: Cigarette smoking has been linked to thyroid disease, although studies of this problem have not shown consistent affects, with some studies linking smoking to increased thyroid hormone levels, and others to decreased thyroid hormone levels. METHODS: We performed a secondary analysis of information collected from 4462 Vietnam-era male US Army veterans aged 31-49 years who participated in the Vietnam Experience Study in 1985-1986. The study group consisted of 1962 current smokers and 2406 current non-smokers who had no thyroid abnormalities on physical examination, no current use of thyroid medicine, and no history of thyroid disease. RESULTS: We found that current smokers have higher thyroxine levels and lower thyroid stimulating hormone levels than never smokers and former smokers. The higher thyroxine levels that we detected in smokers, compared to non-smokers, diminished when we controlled for thyroxine-binding globulin and testosterone. We also found that heavy smokers had a smaller increase in thyroxine levels than did light smokers, when compared to non-smokers. CONCLUSIONS: Our findings suggest at least two distinct mechanisms for the effect of tobacco smoke on thyroid function; one related to higher levels of thyroxine-binding globulin and testosterone among smokers compared to non-smokers and another related to higher levels of thyrotoxins in tobacco smoke in heavy smokers compared to light and moderate smokers.

Lung cancer deaths in the United States from 1979 to 1992: an analysis using multiple-cause mortality data.

BACKGROUND: We sought to describe trends in the presence of lung cancer at the time of death in the United States from 1979 to 1992. METHODS: We analysed death certificate reports in the Multiple-Cause Mortality Files compiled by the National Center for Health Statistics, searching for any mention of lung cancer, lung cancer as the underlying cause of death, and comorbid conditions. RESULTS: Of the 29,042,213 decedents in the study period, 1,892,129 (6.5%) had a diagnosis of lung cancer listed on their death certificates; of these 1,892,129 decedents, 1,734,767 (91.7%) had lung cancer listed as the underlying cause of death. Decedents with lung cancer listed as being present but not the underlying cause of death were more likely to be male (relative risk [RR] 1.16, 95% confidence interval [CI]: 1.15-1.17), and older (RR 4.61, 95% CI: 4.35-4.88 for decedents older than 85 compared to those aged less than 44), but less likely to be black than white (RR 0.88, 95% CI: 0.87-0.90). The mortality rate, age-adjusted to the 1980 population, increased 23.0%, from 47.9 per 100,000 in 1979 to 58.9 per 100,000 in 1992. Over the study period, black men had the highest mortality rates (117.3-125.2 per 100,000), followed by white men (81.7-88.7 per 100,000), men of other races (37.4-46.7 per 100,000), white women (22.1-39.1 per 100,000), black women (21.4-38.2 per 100,000), and women of other races (12.6-18.1 per 100,000). Age-adjusted, state specific rates varied threefold, from 30.4 per 100,000 in Utah to 93.9 per 100,000 in Nevada. CONCLUSIONS: We conclude that the underlying cause of death data base, which captures almost 92% of decedents with lung cancer present, accurately tracks lung cancer mortality trends in the US. Mortality rates of lung cancer, which are decreasing among men, continue to increase among women.

Cystic fibrosis deaths in the United States from 1979 through 1991. An analysis using multiple-cause mortality data.

OBJECTIVE: To analyze mortality trends among people who died with a diagnosis of cystic fibrosis from January 1, 1979, through December 31, 1991. METHODS: We reviewed death certificate reports in the Multiple-Cause Mortality Files compiled by the National Center for Health Statistics. RESULTS: Of the 26,866,600 decedents in the study period, 6500 had a diagnosis of cystic fibrosis listed on their death certificates; of these, 6014 (92.5%) had cystic fibrosis listed as the underlying cause of death. The age-adjusted mortality rate decreased 21%, from 2.4 per 1 million in 1979 to 1.9 per 1 million in 1991, with similar decrements among males and females. The median age of death increased from 15 years in 1979 to 23 years in 1991. During the study period, whites were 6 times more likely to die with a diagnosis of cystic fibrosis than were blacks, and 8 times more likely than were people of other races. Comorbid conditions mentioned on death certificates included obstructive lung disease in 744 (11.5%), pneumonia in 1192 (18.3%), and right heart failure in 986 (15.2%). CONCLUSIONS: From 1979 through 1991, the age-adjusted mortality rate for cystic fibrosis decreased and the median age of death among decedents with a diagnosis of cystic fibrosis increased. These results probably are due to improved treatment of the disease in children, although we cannot exclude other explanations for these findings, such as changes in death certification and coding or better diagnosis of the disease.

Health effects related to environmental tobacco smoke exposure in children in the United States: data from the Third National Health and Nutrition Examination Survey.

OBJECTIVE: To determine the effects of prenatal and postnatal smoke exposure on the respiratory health of children in the United States. DESIGN: Nationally representative cross-sectional survey, including questionnaire information, measurements of serum cotinine (a metabolite of nicotine), and pulmonary function measurement, of 5400 US children. SETTING AND PARTICIPANTS: Children aged 4 to 16 years in the Third National Health and Nutrition Examination Survey, October 25, 1988, to October 15, 1994. METHODS: We stratified the study participants into tertiles, on the basis of serum cotinine levels, and used logistic and linear regression modeling, adjusting for known covariates, to determine the effect of high environmental tobacco smoke (ETS) exposure (on the basis of a high cotinine level) on outcomes such as the prevalence of current asthma, the prevalence of frequent wheezing, school absence, and lung function. For children aged 4 to 11 years, we also determined the effect of prenatal maternal smoking on these outcomes. RESULTS: We observed effects of ETS exposure in all age groups, although the effects varied between age groups. Among all children significant effects associated with high cotinine levels were for wheezing apart from cold in the past year (odds ratio [OR], 1.8; 95% confidence interval [CI], 1.1-2.8); 6 or more days of school absence in the past year (OR, 2.0; 95% CI, 1.4-2.8); and lung function decrements in the forced expiratory volume in 1 second (mean change, -1.8%; 95% CI, -3.2% to -0.4%) and the maximal midexpiratory flow (mean change, -5.9%; 95% CI, -8.1% to -3.4%). Although current and ever asthma were not significantly associated with high cotinine levels in the overall group (OR, 1.5; 95% CI, 0.8-2.7, and OR, 1.3; 95% CI, 0.8-2.2, respectively), they were increased significantly among 4- to 6-year-old children (OR, 5.3; 95% CI, 2.2-12.7, and OR, 2.3; 95% CI, 1.1-5.1, respectively). CONCLUSIONS: We investigated recent ETS exposures as important predictors of respiratory health outcomes in children 4 years and older. Environmental tobacco smoke exposure affects children of all ages, although the exact effects may vary between age groups.

C-reactive protein concentration and concentrations of blood vitamins, carotenoids, and selenium among United States adults.

OBJECTIVE: To examine the relationships between circulating concentrations of C-reactive protein and concentrations of retinol, retinyl esters, vitamin C, vitamin E, carotenoids, and selenium. DESIGN: Cross-sectional study using National Health and Nutrition Examination Survey III (1988-1994) data. SETTING: United States population. SUBJECTS: Up to 14 519 US noninstitutionalized civilian men and women aged > or=20 y. RESULTS: C-reactive protein concentration (dichotomized at the sex-specific 85th percentile) was inversely and significantly associated with concentrations of retinol, retinyl esters, vitamin C, alpha-carotene, beta-carotene, cryptoxanthin, lutein/zeaxanthin, lycopene, and selenium after adjustment for age, sex, race or ethnicity, education, cotinine concentration, body mass index, leisure-time physical activity, and aspirin use. CONCLUSIONS: These results suggest that the inflammatory process, through the production of reactive oxygen species, may deplete stores of antioxidants. Whether increased consumption of foods rich in antioxidants or supplementation with antioxidants can provide health benefits to people characterized by elevated C-reactive protein concentrations may be worthy of further study.

Risk factors for asthma incidence. A review of recent prospective evidence.

AIM: The aim of this study is to determine what factors have been shown, in prospective studies, to predict the incidence of asthma. METHODS: We performed a systematic review of peer-reviewed literature from 1994 to 2004 to determine what factors predict the development of asthma in both children and adults. This search strategy yielded 40 studies, with 36 providing some estimate of asthma incidence for the total sample and or a specific subgroup. RESULTS: Annual estimated incidence of physician-diagnosed asthma ranged from 0.6 to 29.5 per 1000 persons. Risk factors for incident asthma among children included: male sex, atopic sensitization, parental history of asthma, early-life stressors and infections, obesity, and exposure to indoor allergens, tobacco smoke and outdoor pollutants. Risk factors for adult-onset asthma included female sex, airway hyperresponsiveness, lifestyle factors, and work-related exposures. CONCLUSION: Risk factors for asthma include both modifiable and nonmodifiable ones, and they vary between children and adults. This review of prospective evidence supports tobacco and smoke avoidance as an intervention for the primary prevention of childhood asthma. During adolescence and adulthood, targeting lifestyle factors like obesity and smoking or reducing occupational exposures are the best opportunities for asthma prevention. Before specific public health recommendations can be made, however, additional longitudinal research is needed to better characterize target populations and identify appropriate settings for multifaceted asthma interventions.

Emergency department visits and hospitalizations for respiratory disease on the island of Hawaii, 1981 to 1991.

This study examined trends in and patterns of emergency department visits and hospitalizations for respiratory disease on the island of Hawaii from 1981 to 1991. We found that emergency department visit rates and hospitalization rates for both asthma and COPD for 1987 to 1991 increased in all regions of the island in comparison with such rates for 1981 to 1986. Rates of emergency department visits and hospitalizations for chronic obstructive pulmonary disease or COPD, but not asthma, were significantly higher in the high-exposure Kona side of the island than in the intermittent-exposure Hilo side of the island during 1983 and 1988 to 1990. We also found that during the weeks that winds were from the west, blowing volcanic air pollution toward Hilo, emergency department visits for asthma increased 15%. Some of the results of our study support the hypothesis that volcanic air pollution affects respiratory health on the island of Hawaii, while other results do not. Any future studies should include measurements of air pollutant levels.