Outdoor air pollutants have been associated with respiratory effects ranging from changes in lung function1–13 to respiratory symptoms2,3,8,14–16 and cardiopulmonary mortality.2,17–19 However, it is difficult to disentangle the individual effect of each component of the complex mix of ambient aerosol and gases. For many pollutants, indoor concentrations typically are several times higher than outdoor concentrations, particularly in winter when windows and doors are closed tightly and when indoor sources, such as secondary heating devices, are present.20
Secondary heating appliances, such as kerosene heaters, gas space heaters, wood-burning stoves, and fireplaces, are important contributors to indoor air pollution. When these appliances are unvented or poorly vented, they emit many pollutants, including sulfur dioxide (SO2), particulate matter less than 2.5 μm in diameter (PM2.5), strong acid (H+), sulfate (SO42−), carbon monoxide (CO), and nitrogen dioxide (NO2),21–26 into the indoor air. Studies in developed countries have provided equivocal evidence of an association between use of these heating devices and respiratory symptoms.25,27–34 Perhaps a primary shortcoming of previous studies is failure to account for the intermittent use patterns of these heating sources during the heating season.
The design of this study enabled us to specifically examine the effects of secondary heating source use on respiratory symptoms. We test hypotheses that use of fireplaces, wood stoves, kerosene heaters or gas space heaters increases the rate of respiratory symptoms in a group of nonsmoking mothers living in nonsmoking households. We also test hypotheses that measured concentrations of NO2 and SO2 (the primary emissions from these sources) are associated with respiratory symptoms.
Study methods have been described in detail in a previous report on the respiratory health of the infants of mothers in this study.35 After Institutional Review Board approval at each of the hospitals and Yale University, 21,448 mothers delivering babies at 7 hospitals in Connecticut and 5 in southwest Virginia between 1993 and 1996 were screened for study eligibility. Exclusion criteria included any household smoking, infant death or planned adoption, maternal age <19 years, non-English-speaking mother, living or planning to live outside study area, multiple gestation, or having no address or phone number. Screening was designed to provide a study sample overweighted for kerosene heater use, the primary indoor source of SO2. On the basis of reported exposures, 1541 women were invited to participate, including 352 kerosene heater users, 441 gas stove users, 38 users of both, and 709 nonusers who were frequency matched to users on race and delivery hospital. Approximately 20% of these women were no longer eligible at the time of study enrollment (eg, mother resumed smoking or moved in with a smoker), 299 (24%) refused, and 28 (2%) were not enrolled for other reasons, leaving 918 (75%) enrolled. Among enrollees, 221 reported kerosene heater use in the prior winter, and 160 used a kerosene heater during the study period. The current analysis is limited to 888 women for whom symptom information was available during the winter heating season (15 October to 15 April) of their follow-up year (1994–1995 or 1995–1996).
At enrollment, approximately 3–5 months after delivery, each respondent was administered a standardized questionnaire in her home by a trained research assistant. Detailed information was gathered on household demographic data, dwelling characteristics, respondent health status (eg, allergy and asthma status), cooking source (ie, gas or electric), and use of secondary heating sources (ie, fireplaces, wood stoves, gas space heaters, and kerosene heaters).
Respondents recorded daily respiratory symptom information on a calendar provided to them at the initial interview. For one year, women were contacted by telephone approximately every 2 weeks (median interval = 16 days; interquartile range [IQR] = 13–19 days) to obtain information on heating source use during that period and presence of respiratory symptoms on each day during the period. Each contact constituted a reporting period.
Wheezing, phlegm, chest tightness, and laryngitis were considered lower respiratory symptoms; upper respiratory symptoms included runny or stuffy nose, cough, and sore throat. For each day in a reporting period, women reported the presence or absence of each symptom. Reporting period interviews also included a detailed exposure assessment. We obtained information on frequency of use of each secondary heating source during the reporting period. Women reported total number of days and hours that each device was used in the reporting period. Average daily use was calculated separately for each source by multiplying number of heating devices for each source by total hours used, and dividing by days in the period.
Palmes tubes36 were used to passively monitor indoor concentrations of NO2. SO2 concentrations were measured using a passive monitor consisting of a 37-mm diameter polystyrene sampling cassette with a washed glass fiber treated filter coated with a 2% sodium carbonate solution placed at the bottom.37 The filter was analyzed by ion chromatography for SO2 and nitrous acid levels. The monitor was found to measure SO2 over a wide range of concentrations.37
At home interview, the research assistant placed the monitors in the main living area of the home and instructed respondents on their use. Monitors were exposed in the home for 2 weeks, corresponding to the first 2-week symptom reporting period, and then mailed back to our laboratory. Additional monitoring was conducted in the main living area, based on exposure category. Homes with kerosene heaters and gas stoves were monitored for 3 to 6 2-week periods during the winter heating season. Homes with electric stoves and no kerosene heater use received monitoring during 1 2-week period, at initial interview only. Analysis of SO2 and NO2 concentrations is limited to homes monitored at least once during the relevant heating season (n = 589).
Because of the intermittent nature of secondary heater use, data were analyzed by reporting period, rather than averaging over the entire winter heating season, to preserve the linkage between symptom and exposure information. The 888 women followed over the course of a 180-day heating season should provide information for 159,840 person-days; data on exposure or respiratory symptoms were missing for only 1,667 (1%) of those days. The 888 women contributed a total of 9840 reporting periods for a median of 11 reporting periods per woman (IQR = 11–12 periods).
Repeated-measures Poisson regression analysis was performed using a log-linear model in which the response was the number of days during each period in which symptoms were reported. To allow for the varying length of the reporting periods, the log of the period length was introduced as an offset, which effectively results in an analysis of rates, ie, days with symptoms per days of observation. The primary independent variable of interest was average hours per day of reported heating source use during each reporting period, with each source use entered as a continuous variable. Using PROC GENMOD in SAS (SAS Institute, Cary, NC), separate analytic models were run for each respiratory symptom, with the outcome being symptom days per reporting period. Generalized estimating equations were used for handling correlated repeated measures data, and the appropriate structure determined by fitting an m-dependent model in which the only restriction on the working correlation matrix was that the m(= 1–12) lags were identical. These estimated correlations were plotted against the lag, along with those from the AR1 model and from the compound symmetry model. These diagnostic plots suggested that the compound symmetry model gave a good description of the correlation structure for these data, and that it was superior to the AR1 model. Compound symmetry arises from some baseline correlation between observations within an individual, but the correlations are not stronger for observations closer in time.
Although the AR1 model often is considered appropriate for longitudinal data because the correlation varies with lag, we did not find such an effect when the repeated observations were reported by periods. In other work (not reported here) we did find a temporal effect on the working correlation matrix, which usually diminished within a few days to some baseline level, so it is not surprising that we did not find a temporal effect for the relatively long periods which formed the units of analysis of this study. We also assessed the robustness of our findings by repeating the analyses using the AR1 correlation structure, and obtained very similar results. Given the small percentage of missing data, it is assumed to be missing completely at random, and a listwise deletion approach was used in the analysis. Because some respondents used more than 1 heating source during a reporting period, unadjusted and adjusted models included all 4 source use variables, with the reference category being no use of any source. Final adjusted models additionally controlled for respondent's education, race/ethnicity, number of children in the household, other gas sources in the house, type of dwelling (multifamily or single family), respondent's allergy status, and state of residence (Connecticut or Virginia).
We corrected for any overdispersion or extra-Poisson variation by assuming that the variance of the response was proportional to the mean, which was handled by adopting a quasi-likelihood approach. The proportional factor for the variance was estimated by taking the ratio of the Pearson χ2 goodness-of-fit statistic to its degrees of freedom, which was accomplished by using the PSCALE option in GENMOD. The measure of association provided by these analyses is the rate ratio of symptoms per day for each hour-per-day increase in source use.
The aforementioned Poisson regression method described also was used to examine associations of measured concentrations of NO2 and SO2 with counts of each reported respiratory symptom during the passive monitoring period. Women with at least one monitoring of measured concentrations during the winter heating season were included in these analyses (n = 589). Women with gas or kerosene sources received multiple monitoring during the heating season and had repeated observations accounted for in the analysis, as described. These 589 women contributed a total of 1333 monitoring periods. The offset was the log of days in the monitoring period. Because the likelihood of having multiple observations differed depending on exposure status, we repeated the analysis including only the initial monitoring period for all homes (n = 589 monitoring periods).
Overall, 22% of study mothers were African-American or Hispanic, 34% had a high school education or less, and 36% were college graduates (Table 1). Nine percent of women reported a history of physician-diagnosed asthma, and 44% a history of self-reported allergies. Approximately 70% of respondents lived in single-family dwellings. Twenty-one percent of the women had 3 or more children, whereas 41% had only one child.
Among the 888 women in the analysis, 219 (25%) used fireplaces, 25 (3%) gas space heaters, 160 (18%) kerosene heaters, and 155 (17%) wood stoves at least once during the heating season. Fireplace and wood stove users tended to be white and more highly educated, whereas kerosene heater users tended to be less well educated. Use was intermittent during the study period. Among users, fireplaces were used during 25% of their reporting periods, gas space heaters 18%, kerosene heaters 36%, and wood stoves 60% (see details in Triche et al35).
Respiratory symptoms were frequent but episodic among this group of women (Table 2). More than half of the women reported at least 1 day of phlegm, and one third had chest tightness during the study period. Wheezing was much less common, with 9% of women reporting at least 1 day of wheezing. Upper respiratory symptoms were more frequent, with more than 80% of women reporting at least 1 day of runny/stuffy nose, and two thirds reporting cough during the heating season. Symptomatic women reported a specific symptom during 9% to 20% of their reporting periods. The number of days women reported a given symptom during a reporting period ranged from none to all days during that period.
Table 3 presents unadjusted and adjusted rate ratios from Poisson regression models for the associations between hours per day of heating source use and days of lower and upper respiratory symptoms, by reporting period. After controlling for confounders, source use is related to both lower (Table 3, top panel) and upper respiratory (Table 3, bottom panel) symptoms. Fireplace use is associated marginally with chest tightness (RR = 1.05; 0.99–1.12) and phlegm (1.04; 0.99–1.09; Table 3, top panel) and associated with cough (1.05; 1.01–1.09) and sore throat (1.04; 1.00–1.08; Table 3, bottom panel). For every 4-hour per day increase in fireplace use, rates of chest tightness, cough, and sore throat increase approximately 20%. Gas space heater use is modestly associated with a decrease in rate of runny/stuffy nose in unadjusted, but not adjusted models (Table 3, bottom panel). Wood stove use is not associated with any respiratory symptom.
Kerosene heater use is associated with rates of wheezing (1.06; 1.01–1.11; Table 3, top panel); for every 4-hour per day increase in kerosene heater use, there is a 28% increase in rate of wheezing. SO2 concentrations are much higher during monitoring periods in which kerosene heaters were used (Table 4); nonkerosene heater users had virtually no SO2 detected in their homes. Median levels of SO2 in monitoring periods with kerosene heater use are 30 times higher compared with periods with no use. Measured concentrations of NO2, too, are much higher during monitoring periods in which gas space heaters are used (Table 4), but there is more variability in NO2 concentrations in non-gas heater periods.
Measured concentrations of SO2 are associated with wheezing (1.57; 1.10–2.26 for every 10 ppb increase in SO2) and chest tightness (1.32; 1.01–1.71), but not other symptoms, when controlling for NO2 and confounders (Table 5). When the analysis is limited to the first monitoring period, SO2 remains associated with wheezing (2.00; 1.38–2.91 per 10 ppb increase) and chest tightness (1.83; 1.15–2.92 per 10 ppb increase) and also is associated with runny/stuffy nose and cough. NO2 concentrations are not associated with any respiratory symptom in these models. However, when NO2 exposure is dichotomized as 80 ppb or greater (top quartile for users), it is associated with chest tightness (1.94; 0.98–3.85) and strongly associated with wheezing (4.00; 1.45–11.0; data not shown).
This study provides evidence that short-term exposure to secondary heating devices and their emissions increases rates of acute respiratory symptoms among nonsmoking women living in nonsmoking households. The study is one of few prospective studies specifically designed to address these associations. Study strengths include extensive information on potential confounders, prospectively collected information on respiratory symptoms, frequent ascertainment of source use information, and large sample of nonsmoking women in households with no passive smoke exposure.
The ability to account for intermittent use of secondary heating sources is a novel contribution of this research. Even within the same homes, use of these heating devices is episodic and varies widely over the winter heating season. Rather than averaging hours of use over an entire heating season (which would dilute any effects), we assessed use patterns over a shorter reporting period (approximately 2 weeks) in relation to symptoms during that same period. An additional strength of the study is the measurement of specific emissions from some of these heating sources.
The primary limitation of the study is that the symptom and source use data are self-reported. Although some misclassification may have occurred, frequent follow-up should have reduced possible misclassification by limiting the period of recall. Any misclassification should be nondifferential and tend to reduce effect sizes. Another limitation of the study is concurrent ascertainment of exposure and outcome data, making it difficult to confirm the temporal direction of the reported associations. Although women were given a calendar and asked to record symptoms daily, they were not asked dates of source use within a given reporting period. Patterns of kerosene heater use do not appear to be in response to symptoms. Of the 159 users, 42 had only one reporting period with kerosene heater use, but only 11 of these had symptoms in that period. Of the 117 women with more than one reporting period with kerosene heater use, 78 did not have symptoms in the reporting period in which the heater was first used. Most women began using kerosene heaters after the onset of the heating season, apparently unrelated to symptoms. Moreover, the specificity of the association between kerosene heater use and wheezing further supports the assertion that use of sources was not in response to symptoms; it is unlikely that wheezing, but not other symptoms, resulted in use of kerosene heaters.
Extensive chamber studies have found that kerosene heaters are an almost exclusive indoor source of sulfate aerosol (SO42−), as well as an important source of PM2.5 and acid aerosol (H+).20,22 Active monitoring of indoor particles on a subset of 74 study homes allowed us to calculate indoor PM2.5 and SO42− levels from measured SO2 concentrations associated with kerosene heater use in this population, and they are comparable to those levels typically encountered in outdoor air.20 The specific association between SO2 and sulfate particles from these study homes is shown in Figure 4 of the article by Leaderer et al20 In these study homes, kerosene heaters are an almost exclusive source of SO2—and thus sulfate aerosol—in the indoor environment.
Animal studies have determined that kerosene heater exposure increases bronchoconstriction.38–41 The small number of studies on the effects of kerosene exposure in humans have focused primarily on accidental ingestion or poisoning with liquid kerosene, which has been associated with pneumonia, pulmonary edema,26 asthma, and lower and upper respiratory symptoms.42 However, our findings are in agreement with a recent epidemiologic study by Venn et al,43 who found that kerosene heater use in an urban Ethiopian population increased wheezing and rhinitis, adjusting for age, sex, and socioeconomic status. Kerosene heater use was associated with increased rate of wheezing among the women in our study. Our findings of an association between measured concentrations of SO2 and chest tightness and wheezing among women monitored during the heating season add support to the hypothesis that sulfate particles emitted from kerosene heaters are associated with acute respiratory symptoms.
Fireplace use, but not wood stove use, was associated with increased rates of cough, sore throat, and chest tightness in this study. Fireplaces, as compared with wood stoves, may be less well vented or less tightly closed and may emit more particles and combustion gases directly into indoor air. In a previous work on the respiratory symptoms of the infants of these women,35 wood stoves but not fireplaces were associated with infant cough. This may be attributable in part to fireplaces being used by parents after the infants have gone to bed (ie, more for relaxation than heating), as suggested by the differences in average use of fireplaces (mean, 1.6 hours per day) compared with wood stove (mean, 11.5 hours per day) use.
Wood-burning appliances, such as fireplaces, emit a complex mix of particles of varying chemical and physical composition. The average particle size is less than 1 μm, which can easily penetrate deeply into the respiratory tract.25 Evidence exists that these particles irritate the upper airways44,45 and interfere with ciliary action.25 Animal studies demonstrate that exposure to wood smoke may decrease ventilatory function, increase pulmonary edema, and compromise the pulmonary immune system. Prolonged or repeated wood smoke exposure in humans has been related to chronic effects, including chronic bronchitis, interstitial lung disease and pulmonary arterial hypertension.26,46 We did not assess long-term effects of cumulative exposures in this study.
In developing countries, where wood smoke exposure tends to be more intense, acute respiratory health effects in women and children have been noted, but similar studies in developed countries have been equivocal.25,27–29,31 Few studies on the acute health effects of wood smoke exposure among adults are available; however, our findings tend to be consistent with these studies. Heavy exposure among charcoal workers was linked to short-term effects, such as increased cough, wheezing, and sputum production, as well as decreased lung function.47 Similarly, forest firefighters exposed to high levels of smoke experienced declines in lung function across work shifts and seasons, as well as decreased lung function associated with indoor wood smoke exposure. Ellegard28 found an increase in cough among 1200 randomly selected women in a Mozambique suburb, controlling for environmental variables. Lipsett et al48 observed that indoor wood smoke exposure increased the likelihood of shortness of breath in women and men living in Denver and increased the likelihood of cough in men.
Findings related to the use of gas space heaters and respiratory symptoms suggest an association with wheezing, although gas space heaters were used in only 25 homes, limiting the power to detect an association. Only high measured concentrations of NO2 (≥80 ppb; top quartile among users) were associated with wheezing and chest tightness. Previous findings of an association between nitrogen dioxide and respiratory symptoms have been inconsistent.30,32–34 However, there is a paucity of studies examining acute respiratory effects of gas source use or gas phase emissions from these sources in a population of healthy nonsmoking adults. Our findings suggest that among this population, gas phase emissions may have an acute effect on lower respiratory symptoms, which are consistent with findings of the infants of these mothers in which gas space heater use was found to increase rates of wheezing in the first year of life.35
Our observations strengthen previous findings of an association between indoor heating source use and respiratory symptoms by prospectively examining the relationship in a population of nonsmoking women in the United States while accounting for intermittent source use patterns. Although severity of symptoms was not determined in this study, the findings indicate that use of portable kerosene heaters, gas space heaters, and fireplaces increase the rate of respiratory symptoms, including wheezing and chest tightness, in nonsmoking women living in households with no passive smoke exposure. The findings are further supported by the observed association between measured concentrations of source emissions and chest tightness and wheezing.
We thank the 918 families in Virginia and Connecticut who provided extensive information over the first year of their infants’ lives. We also thank the following hospitals, from which our study population was selected: In Connecticut–Danbury Hospital, Manchester Memorial Hospital, Middlesex Memorial Hospital, William W. Backus Hospital, Veterans Memorial Medical Center, and Yale-New Haven Hospital; in Virginia–Community Hospital (Roanoke), Danville Regional Medical Center, Martha Jefferson Hospital (Charlottesville), University of Virginia Health Sciences Center, and Virginia Baptist Hospital (Lynchburg).
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