Long-term Particulate and Other Air Pollutants and  Lung Function in Nonsmokers

Abbey, David E.; Burchette, Raoul J.; Knutsen, Synnøve F.; McDonnell, William F.; Lebowitz, Michael D.; Enright, Paul

doi:10.1164/ajrccm.158.1.9710101

Cited by 173 publications

(127 citation statements)

References 31 publications

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“…Two other observational studies demonstrated a relation between ETS exposure and decreased forced expiratory flow, midexpiratory phase (FEF 25%-75% ), but not FEV 1 or FVC (35,36). Other investigators have found no consistent relationship between ETS exposure and pulmonary function in adults (37)(38)(39)(40)(41)(42)(43)(44)(45)(46).…”

Section: Discussionmentioning

confidence: 98%

Environmental tobacco smoke exposure and pulmonary function among adults in NHANES III: impact on the general population and adults with current asthma.

Eisner

2002

Environ Health Perspect

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The impact of environmental tobacco smoke (ETS) exposure on adult pulmonary function has not been clearly determined. Because adults with asthma have chronic airway inflammation, they may be a particularly susceptible group. Using data from the Third National Health and Nutrition Examination Survey (NHANES III), I examined the cross-sectional relationship between serum cotinine, a biomarker of ETS exposure, and pulmonary function among 10,581 adult nonsmokers and 440 nonsmoking adults with asthma whose cotinine and spirometry data were available. I generated residuals, which are observed minus predicted values (based on Crapo equations), for forced expiratory volume in 1 sec (FEV1), forced vital capacity (FVC), and FEV1/FVC ratio to adjust for age, sex, and height. In addition, I used multivariate linear regression to control for sociodemographic characteristics and previous smoking history. Most adults with and without asthma had detectable serum cotinine levels, indicating recent ETS exposure (85.7% and 83.4%, respectively). Among nonsmoking male participants, I found no evidence that ETS exposure was related to decreased pulmonary function. In the nonsmoking female stratum, the highest cotinine tertile was associated with a lower FEV1 [-100 mL; 95% confidence interval (CI), -143 to -56 mL], FVC (-119 mL; 95% CI, -168 to -69 mL), and FEV1/FVC ratio (-1.77%; 95% CI, -2.18% to -1.36%). Among women with asthma, the highest cotinine tertile was also associated with decreased FEV1 (-261 mL; 95% CI, -492 to -30 mL), FVC (-291 mL; 95% CI, -601 to 20 mL), and FEV1/FVC ratio (-1.6%; 95% CI, -3.3% to 0.19%). In conclusion, ETS exposure is associated with decreased pulmonary function in adult females, especially those with asthma. This analysis should provide further impetus for public policies that promote smoke-free environments.

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Section: Discussionmentioning

confidence: 98%

Environmental tobacco smoke exposure and pulmonary function among adults in NHANES III: impact on the general population and adults with current asthma.

Eisner

2002

Environ Health Perspect

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“…The risk of asthma onset or chronic effects on asthma from ambient air pollution exposure has been less clearly identified in epidemiologic studies, although few studies are prospective cohort designs (6)(7)(8)(9)(10)(11)(12)(13). A cohort study of nonsmoking adult Seventh Day Adventists in California followed 10 or more years found associations between the development of asthma and outdoor concentrations of total suspended particulates (11), total suspended sulfate (12), and ozone (O 3 ) (13).…”

Section: Importancementioning

confidence: 99%

Epidemiologic evidence for asthma and exposure to air toxics: linkages between occupational, indoor, and community air pollution research.

Delfino

2002

Environ Health Perspect

269

152

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Outdoor ambient air pollutant exposures in communities are relevant to the acute exacerbation and possibly the onset of asthma. However, the complexity of pollutant mixtures and etiologic heterogeneity of asthma has made it difficult to identify causal components in those mixtures. Occupational exposures associated with asthma may yield clues to causal components in ambient air pollution because such exposures are often identifiable as single-chemical agents (e.g., metal compounds). However, translating occupational to community exposure-response relationships is limited. Of the air toxics found to cause occupational asthma, only formaldehyde has been frequently investigated in epidemiologic studies of allergic respiratory responses to indoor air, where general consistency can be shown despite lower ambient exposures. The specific volatile organic compounds (VOCs) identified in association with occupational asthma are generally not the same as those in studies showing respiratory effects of VOC mixtures on nonoccupational adult and pediatric asthma. In addition, experimental evidence indicates that airborne polycyclic aromatic hydrocarbon (PAH) exposures linked to diesel exhaust particles (DEPs) have proinflammatory effects on airways, but there is insufficient supporting evidence from the occupational literature of effects of DEPs on asthma or lung function. In contrast, nonoccupational epidemiologic studies have frequently shown associations between allergic responses or asthma with exposures to ambient air pollutant mixtures with PAH components, including black smoke, high home or school traffic density (particularly truck traffic), and environmental tobacco smoke. Other particle-phase and gaseous co-pollutants are likely causal in these associations as well. Epidemiologic research on the relationship of both asthma onset and exacerbation to air pollution is needed to disentangle effects of air toxics from monitored criteria air pollutants such as particle mass. Community studies should focus on air toxics expected to have adverse respiratory effects based on biological mechanisms, particularly irritant and immunological pathways to asthma onset and exacerbation.

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“…Time series studies (Pope et al, 1992;Schwartz, 1994aSchwartz, ,b, 1997Schwartz, , 1999Schwartz and Dockery, 1992;BorjaAburto et al, 1998 ) of acute impacts have been complemented by evidence from prospective cohort studies ( Dockery et al, 1993;Pope et al, 1995a,b;Abbey et al, 1998 ). To support these epidemiological associations, much current research is focused on the elucidation of biologically plausible mechanisms through which airborne particles may act ( NRC, 1998 ) .…”

Section: Introductionmentioning

confidence: 99%

Exposure of chronic obstructive pulmonary disease patients to particles: Respiratory and cardiovascular health effects

Bräuer

Ebelt

Fisher

et al. 2001

J Expo Sci Environ Epidemiol

109

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To examine hypotheses regarding air pollution health effects, we conducted an exploratory study to evaluate relationships between personal and ambient concentrations of particles with measures of cardiopulmonary health in a sample of patients with chronic obstructive pulmonary disease ( COPD ) . Sixteen currently non -smoking COPD patients ( mean age = 74 ) residing in Vancouver were equipped with a particle ( PM 2.5 ) monitor for seven 24 -h periods. Subjects underwent ambulatory heart monitoring, had their lung function and blood pressure ( BP ) measured, and recorded symptoms and medication use. Ambient PM 2.5 , PM 10 , sulfate, and gaseous pollutant concentrations were monitored at five sites within the study area. Although no associations between air pollution and lung function were statistically significant, an estimated effect of 3% and 1% declines in daily FEV 1 change ( ÁFEV 1 ) for each 10 g / m 3 increase in ambient PM 10 and PM 2.5 , respectively, was observed. Increases of 1 g / m 3 in personal or ambient sulfate were associated with 1.0% and 0.3% declines in ÁFEV 1 , respectively. Weak associations were observed between particle concentrations and increased supraventricular ectopic heartbeats and with decreased systolic BP. No consistent associations were observed between any particle metric and diastolic BP, heart rate, or heart rate variability ( r -MSSD or SDNN ) , symptom severity, or bronchodilator use. Of the pollutants measured, ambient PM 10 was most consistently associated with health parameters; the use of personal exposures did not improve the strength of any associations or lead to increased effect estimates.

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Long-term Particulate and Other Air Pollutants and Lung Function in Nonsmokers

Cited by 173 publications

References 31 publications

Environmental tobacco smoke exposure and pulmonary function among adults in NHANES III: impact on the general population and adults with current asthma.

Environmental tobacco smoke exposure and pulmonary function among adults in NHANES III: impact on the general population and adults with current asthma.

Epidemiologic evidence for asthma and exposure to air toxics: linkages between occupational, indoor, and community air pollution research.

Exposure of chronic obstructive pulmonary disease patients to particles: Respiratory and cardiovascular health effects

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