Abstract
Objective:
To evaluate the impact of exposure to indoor air pollution on respiratory health outcomes (healthcare utilization, symptoms, medication use) in infants and children with bronchopulmonary dysplasia (BPD).
Study design:
244 subjects were included from the Johns Hopkins BPD registry. Parents completed an environmental exposure questionnaire including secondhand smoke and indoor combustion (gas/ propane heat, gas or wood stove, gas/ wood burning fireplace) exposures in the home. Acute (healthcare utilization, steroid / antibiotic use) and chronic respiratory symptoms (cough/ wheeze, nocturnal cough, use of beta-agonists, tolerance of physical activity) were also collected.
Results:
Three-quarters of infants were exposed to at least one combustible source of air pollution in the home and this exposure was associated with increased risk of hospitalization in infants and children on home respiratory support. Only 14% of the study population reported SHS exposure but we found that this was associated with chronic respiratory symptoms, including activity limitation and nocturnal cough. Infants on respiratory support additionally had increased daytime cough and wheezing. Approximately one-third reported having an air purifier in the home and its presence attenuated the effect of SHS exposure on reported activity limitation.
Conclusions:
Exposure to combustible sources of indoor air pollution was associated with increased respiratory morbidity in a group of high risk of infants with BPD. Our results support that indoor air pollution is a modifiable risk factor for respiratory health in infants with BPD.
Keywords: chronic lung disease of prematurity, premature birth, combustion, secondhand smoke, home environment, particulate matter, nitrogen dioxide
Premature birth affects approximately 10% of infants born in the U.S. and is the leading cause of infant mortality.(1) Bronchopulmonary dysplasia (BPD), characterized by impaired alveolar growth and lung injury, is one of the most common and serious complications of preterm birth occurring in 40% of infants born between 22 and 28 weeks gestation. (2, 3) Although children with BPD can exhibit alveolar catch-up growth during childhood,(4) early life exposures such as tobacco smoke can adversely impact long-term trajectories in lung function.(5)
The U.S. Environmental Protection Agency has concluded that fine particle pollution (PM2.5) is a serious health threat based on its association with multiple adverse health effects.(6) For infants and children, exposure to indoor or outdoor sources of PM2.5 has been linked to respiratory related infant mortality (7), development of asthma,(8) slowed lung function growth,(9) and increased asthma morbidity.(10) Exposure to Nitrogen Dioxide (NO2, a gaseous air pollutant that results from combustion) also has harmful effects on the lungs including increased inflammation, cough, and asthma exacerbations.(11) Although secondhand smoke exposure (a major source of indoor air pollution when present) has been associated with increased hospitalizations for respiratory illnesses in infants and children with BPD,(12) little is known about the health effects of air pollution exposure specifically in this vulnerable population. Because management of these infants focuses on minimizing further lung injury, identifying and minimizing modifiable risk factors such as environmental exposures is of critical importance. In this study, we hypothesized that parent reported exposures to indoor air pollution at home would be associated with increased healthcare utilization, symptoms, and medication use.
METHODS
The subjects (n=244) in this study were recruited from the Johns Hopkins Bronchopulmonary Dysplasia Clinic during routine follow-up visits between April 2016 and October 2018. The Bronchopulmonary Dysplasia Patient registry is a cohort of approximately 900 infants and children which actively collects respiratory health data at each pulmonary follow up visit, thus providing an opportunity to investigate the influence of air pollution exposures on clinical outcomes. Patients seen in clinic were referred from at least 13 NICUs across the state of Maryland. Inclusion criteria included being born preterm (<32 weeks gestation) and being diagnosed with BPD per National Institute of Child Health and Human Development NICHD criteria.(13) This study was approved by the Johns Hopkins Institutional Review Board (protocol #NA_051884). All parents and caregivers were orally consented per IRB.
Clinical and demographic data were obtained through chart review. Race/ethnicity was self-reported; for the purposes of analysis, subjects that reported having any non-white ancestry were coded as non-white. Median household income was derived from 2010 US Census data based on residential zip code (U.S. median household income: $50,502; State of Maryland median household income: $70,004). Health insurance information was obtained from billing records. Birth weight percentiles reflect birth weights corrected for gestational age.(14)
The environmental exposure questionnaire is an unvalidated set of questions adapted from the Johns Hopkins Center for Childhood Asthma in the Urban Environment. Subjects were classified as having indoor smoking exposure if caregivers reported that smoking occurred inside the home or smoking occurred inside a shared building (e.g., apartment building) within the past 3 months. Subjects were classified as having exposure to indoor combustion if caregivers reported the presence of gas or propane heat, gas or wood stoves, and/or gas or wood fireplaces within the home. These exposures and the use of air purifiers were only determined to be present or absent; use patterns were not captured. Only one environmental questionnaire per subject was completed.
Acute respiratory outcomes (eg, emergency department visits and hospitalizations for respiratory symptoms, steroid courses, antibiotic courses for respiratory illnesses over the preceding 2 months) and chronic respiratory symptoms (e.g. coughing/wheezing, nighttime cough, use of short-acting beta-agonists at home, shortness of breath with play or activities over the past week) were collected via an unvalidated questionnaire at routine follow-up clinic visits. Currently, validated instruments for outpatients with bronchopulmonary dysplasia are not available. A total of 865 outcome questionnaires were completed for 244 subjects with 2.1% of all questions left blank by caregivers (Mean number of questionnaires per subject: 3.5±3.6; Range: 1–25).
Statistical Analyses:
Differences for demographic and clinical factors between subjects exposed to indoor smoking and/or combustion compared with those who were not were assessed using the appropriate parametric tests (χ2 and t tests). The relationships between respiratory morbidities (dependent variable) and self-reported environmental exposures (independent variable) were assessed using multivariable logistic regression to generate odds ratios adjusted for the age of the subject at the time of environmental and clinical questionnaire completion, and clinical/demographic factors that differed by self-reported exposures (specifically race/ethnicity and insurance status for indoor smoking and median household income for indoor combustion). As caregivers may have completed outcomes questionnaires at several clinic visits, the logistic regressions accounted for the possibility of more than one questionnaire per subject using Generalized Estimating Equations methodology (clustered by subject)(15). To assess the effects of the presence of an air purifier in the home, logistic regressions were re-run only for outcomes associated with exposures stratified by the presence of an air purifier. Kaplan-Meier methodology was used to analyze the time at which subjects on home supplemental oxygen via nasal cannula were weaned off oxygen stratified by exposures and unadjusted for other factors. All statistical analyses were conducted using Stata IC 15.0 (College Station, TX). P values <0.05 were considered statistically significant.
RESULTS
A total of 244 subjects completed environmental exposure questionnaires with a mean age of 2.3 years at form completion (Table I). Subjects were 44.3% female, born at a mean gestational age of 26.8 weeks, and were discharged to home for the first time at a mean age of 4.9 months of age. A total of 14.3% of caregivers reported indoor smoking exposure within the past 3 months, including 3.7% within the living space and 12.1% within a shared building (Table 2). A total of 75.8% reported at least one combustion source indoors with the most common sources being gas stoves (50.2%) and gas heat (43.2%). Those exposed to indoor smoking were more likely to be non-white (80.0% vs. 60.8%; P = .03) and to be covered by public insurance (71.4% vs. 50.2%; p=0.02) compared with those not exposed (Table 1). Those exposed to indoor combustion had a higher median household income ($67,587 vs $60,438; p=0.031) compared with those not exposed (Table 3). There were no other significant differences in clinical or demographic factors between those exposed to smoking/combustion versus those not exposed.
Table 1.
Study Population Demographics by Reported Indoor Smoking
| Mean ± S.D. [Range] | Entire Population (n = 244) | Reported Indoor Smoking (n = 35) | No Reported Indoor Smoking (n = 209) | P Value | |
|---|---|---|---|---|---|
| Demographics | Age at Form Completion (Y ears) | 2.3 ± 2.6 [0.2, 16.4] |
1.7 ± 1.7 [0.3, 7.2] |
2.4 ± 2.7 [0.2, 16.4] |
0.12 |
| Sex (% female) | 44.3 | 45.7 | 44.0 | 0.85 | |
| Race/Ethnicity (% non-white) | 63.5 | 80.0 | 60.8 | 0.029 | |
| Gestation (weeks) | 26.8 ± 2.4 [22.9 – 32] |
26.2 ± 2.4 [23 – 32] |
26.9 ± 2.3 [22.9 – 32] |
0.10 | |
| Birth Weight (grams) | 921 ± 354 [380 – 2310] (n = 243) |
875 ± 310 [480 – 2188] |
929 ± 361 [380 – 2310] (n = 208) |
0.41 | |
| Birth Weight (Percentile) | 41.6 ± 25.8 [1 – 94] (n = 243) |
48.9 ± 28.7 [2 – 94] |
40.4 ± 25.1 [1 – 92] (n = 208) |
0.07 | |
| Median Household Income ($ 000’s) | 65.9 ± 22.2 [21.9 – 132.7] |
63.1 ± 19.7 [28.9 – 103.6] |
66.3 ± 22.6 [21.9 – 132.7] |
0.42 | |
| Public Insurance (% yes) | 53.3 | 71.4 | 50.2 | 0.020 | |
| Clinical Data | Age at Discharge from NICU (Months) | 4.9 ± 3.5 [0.5 – 26.5] (n = 243) |
4.4 ± 2.5 [0.7 – 15.0] |
4.8 ± 3.5 [0.5 – 26.5] (n = 208) |
0.49 |
| Home Supplemental Oxygen (% yes) | 45.5 | 45.7 | 45.5 | 0.98 | |
| Home Ventilator (% yes) | 6.2 | 8.6 | 5.7 | 0.52 | |
| Gastrostomy Tube (% yes) | 32.0 | 34.3 | 31.6 | 0.75 | |
| Ventricular Shunt (% yes) | 10.3 | 8.6 | 10.5 | 0.72 | |
| Inhaled Corticosteroid Use Prior to Age 2yo (% yes) | 81.6 | 82.9 | 81.3 | 0.83 | |
| Air Purifier in Home (% yes) | 33.3 (n = 243) |
31.4 | 33.7 (n = 208) |
0.80 | |
Table 2.
Indoor Environmental Exposures
| (% Yes) | Entire Population (n = 244) | |
|---|---|---|
| Smoking Exposures | Smoking inside living space within the past 3 months | 3.7 |
| Smoking inside shared building within the past 3 months (n = 224) | 12.1 | |
| Any reported smoking inside | 14.3 | |
| Combustion Exposures | Gas stove (n = 243) | 50.2 |
| Wood stove (n = 243) | 0.4 | |
| Gas heating (n = 220) | 43.2 | |
| Propane heating (n = 220) | 2.7 | |
| Gas fireplace (n = 243) | 11.5 | |
| Wood fireplace | 17.6 | |
| Any of the above combustion sources | 75.8 | |
| Air Purifier | Present in home (n = 243) | 33.3 |
Table 3.
Study Population Demographics by Reported Indoor Combustion Sources
| Mean ± S.D. [Range] | Entire Population (n = 244) | Reported Indoor Combustion (n = 185) | No Reported Indoor Combustion (n = 59) | P Value | |
|---|---|---|---|---|---|
| Demographics | Age at Form Completion (Y ears) | 2.3 ± 2.6 [0.2, 16.4] |
2.5 ± 2.7 [0.2, 16.4 |
1.8 ± 2.1 [0.2, 9.2] |
0.10 |
| Sex (% female) | 44.3 | 41.6 | 52.5 | 0.14 | |
| Race/Ethnicity (% non-white) | 63.5 | 62.7 | 66.1 | 0.64 | |
| Gestation (weeks) | 26.8 ± 2.4 [22.9 – 32] |
26.8 ± 2.4 [22.9 – 32] |
26.8 ± 2.2 [23 – 31.3] |
0.88 | |
| Birth Weight (grams) | 921 ± 354 [380 – 2310] (n = 243) |
935 ± 364 [380 – 2310] (n = 184) |
879 ± 317 [380 – 1800] |
0.29 | |
| Birth Weight (Percentile) | 41.6 ± 25.8 [1 – 94] (n = 243) |
42.3 ± 25.5 [1 – 94] (n = 184) |
39.3 ± 26.7 [2 – 89] |
0.44 | |
| Median Household Income ($ 000’s) | 65.9 ± 22.2 [21.9 – 132.7] |
67.6 ± 22.3 [25.2 – 132.7] |
60.4 ± 21.2 [21.9 – 108.1] |
0.031 | |
| Public Insurance (% yes) | 53.3 | 54.1 | 50.9 | 0.67 | |
| Clinical Data | Age at Discharge from NICU (Months) | 4.9 ± 3.5 [0.5 – 26.5] (n = 243) |
4.9 ± 3.5 [0.5 – 26.5] (n = 184) |
4.4 ± 2.7 [0.9 – 14.3] |
0.30 |
| Home Supplemental Oxygen (% yes) | 45.5 | 46.0 | 44.1 | 0.80 | |
| Home Ventilator (% yes) | 6.2 | 6.0 | 6.8 | 0.82 | |
| Gastrostomy Tube (% yes) | 32.0 | 34.6 | 23.7 | 0.12 | |
| Ventricular Shunt (% yes) | 10.3 | 11.9 | 5.1 | 0.13 | |
| Inhaled Corticosteroid Use Prior to Age 2yo (% yes) | 81.6 | 81.6 | 81.4 | 0.96 | |
| Air Purifier in Home (% yes) | 33.3 (n = 243) |
34.2 (n = 184) |
30.5 | 0.60 | |
Respiratory Outcomes:
Clustered logistic regressions adjusted for age at the time of form completion and other confounders were used to test for association between indoor smoking/combustion and acute/chronic respiratory outcomes (Table 4). Reported indoor smoking was found to be associated with several chronic respiratory symptoms, including a 2.0-fold increase in activity limitations (p=0.05) and a 2.4-fold increase in nighttime symptoms (p=0.03). These findings were more severe in subjects requiring respiratory support in the home setting (defined as oxygen, ventilator, and/or tracheostomy dependence at initial NICU discharge) with a 2.9-fold increase in coughing/wheezing (p=0.01), a 4.3-fold increase in activity limitations (p=0.004) and a 6.5-fold increase in nighttime symptoms (p=0.001). Acute care use and rescue beta-agonist use were not found to be associated with reported indoor smoking. Reported indoor combustion tended to be associated with an increased risk of inpatient hospitalization after initial NICU discharge (adjusted OR: 2.2; p=0.06), and this risk was again more pronounced in subjects requiring respiratory support at home (adjusted OR: 6.0; p=0.04) (Table 4).
Table 4.
Reported Indoor Smoking as a Predictor of Selected Respiratory Outcomes
| All Subjects | Subjects on Home Respiratory Support** | |||||
|---|---|---|---|---|---|---|
| Odds Ratio* [95% C.I.] | N | P Value | Odds Ratio [95% C.I.] | N | P Value | |
| Emergency Department Visit | 1.40 [0.67, 2.92] |
244 (860 forms) | 0.37 | 1.54 [0.66, 3.60] |
114 (449 forms) | 0.32 |
| Inpatient Hospitalization | 0.97 [0.43, 2.21] |
244 (860 forms) | 0.95 | 1.19 [0.46, 3.04] |
114 (449 forms) | 0.72 |
| Systemic Steroid Use | 1.23 [0.56, 2.72] |
244 (857 forms) | 0.61 | 1.37 [0.51, 3.65] |
114 (446 forms) | 0.54 |
| Antibiotic Use | 1.64 [0.72, 3.75] |
244 (852 forms) | 0.24 | 1.70 [0.47, 6.18] |
114 (443 forms) | 0.42 |
| Cough or Wheeze | 1.45 [0.77, 2.74] |
243 (852 forms) | 0.25 | 2.89 [1.24, 6.74] |
114 (446 forms) | 0.014 |
| Rescue β-agonist Use | 1.78 [0.88, 3.61] |
244 (829 forms) | 0.11 | 2.31 [0.85, 6.24] |
114 (434 forms) | 0.10 |
| Activity Limitations | 1.98 [1.00, 3.91] |
244 (817 forms) | 0.050 | 4.26 [1.59, 11.41] |
114 (427 forms) | 0.004 |
| Nighttime Symptoms | 2.43 [1.12, 5.29] |
244 (850 forms) | 0.025 | 6.45 [2.05, 20.26] |
114 (444 forms) | 0.001 |
| Reported Indoor Combustion Sources as a Predictor of Selected Respiratory Outcomes | ||||||
| All Subjects | Subjects on Home Respiratory Support** | |||||
| Odds Ratio* [95% C.I.] | N | P Value | Odds Ratio* [95% C.I.] | N | P Value | |
| Emergency Department Visit | 1.60 [0.84, 3.06] |
244 (860 forms) | 0.16 | 2.42 [0.92, 6.37] |
114 (449 forms) | 0.07 |
| Inpatient Hospitalization | 2.20 [0.96, 5.05] |
244 (860 forms) | 0.06 | 5.95 [1.08, 32.76] |
114 (449 forms) | 0.040 |
| Systemic Steroid Use | 1.34 [0.86, 2.07] |
244 (857 forms) | 0.20 | 1.44 [0.71, 2.95] |
114 (446 forms) | 0.31 |
| Antibiotic Use | 0.84 [0.48, 1.50] |
244 (852 forms) | 0.57 | 1.78 [0.77, 4.15] |
114 (443 forms) | 0.18 |
| Cough or Wheeze | 1.21 [0.76, 1.92] |
243 (852 forms) | 0.42 | 1.39 [0.66, 2.94] |
114 (446 forms) | 0.39 |
| Rescue β-agonist Use | 1.02 [0.65, 1.61] |
244 (829 forms) | 0.92 | 0.85 [0.43, 1.69] |
114 (434 forms) | 0.64 |
| Activity Limitations | 1.18 [0.74, 1.88] |
244 (817 forms) | 0.50 | 0.97 [0.44, 2.11] |
114 (427 forms) | 0.94 |
| Nighttime Symptoms | 1.64 [0.93, 2.89] |
244 (850 forms) | 0.09 | 2.24 [0.60, 8.45] |
114 (444 forms) | 0.23 |
Odds ratios for respiratory outcomes (dependent variable) given reported indoor smoking (independent variable) were generated through logistic regression clustered by subject and adjusted for potential confounders, including race/ethnicity, insurance status, age at the time of environmental assessment, and age at the time of respiratory outcomes questionnaire completion.
Of the 244 subjects in this study, 98 were on supplemental oxygen via nasal cannula, 15 were on home ventilators, and 1 had a tracheostomy without ventilator or oxygen use. Odds ratios were calculated in a similar manner to the all subjects regressions.
Indoor Pollution Mitigation:
To test whether the presence of an air purifier in the home affected outcomes, logistic regressions that were significant for associations between indoor air pollution and respiratory outcomes as observed above were re-run stratified by the presence of an air purifier. Within the study population 33.3% of caregivers reported having an air purifier in the home. The previously observed association between indoor smoking and activity limitations/nighttime symptoms was not present when an air purifier was reported to be present (Table 5; available at www.jpeds.com). Specifically, there was a 2.6-fold increased risk of activity limitations (p=0.01) and a 2.3-fold increased risk of nighttime symptoms (p=0.06) with indoor smoking when an air purifier was not present versus non-significant adjusted odds ratios for activity limitations (p=0.98) and for nighttime symptoms (p=0.18) when it was. Likewise, similar findings were seen when examining only subjects on home respiratory support with the presence of an air purifier appearing to mitigate associations (Table 6; available at www.jpeds.com). Specifically, there was a 2.3-fold increased risk of cough/wheeze (p=0.08) and a 3.7-fold increased risk of activity limitations (p=0.02) with indoor smoking when an air purifier was not present versus non-significant odd ratios for cough/wheeze (p=0.18) and for activity limitations (p=0.11) when it was. Reported indoor smoking remained associated with an over 6-fold risk of nighttime symptoms in subjects on home respiratory support regardless of whether an air purifier was present (p=0.05) or not (p=0.005). As all subjects on respiratory support reporting indoor combustion and the presence of an air purifier also reported hospitalization, the regressions could not be performed for this outcome and exposure. Although questionnaires did ascertain whether a stove exhaust fan was present (as a mitigating factor for indoor combustion from gas stoves), of the 121 caregivers that reported a gas stove was present, the majority (88.4%) also reported that a stove exhaust fan was present, thus leading to likely underpowering of any such analyses.
Table 5.
Presence of Air Purifiers as a Modifier of Selected Respiratory Outcomes
| No Air Purifier | Air Purifier | ||||||
|---|---|---|---|---|---|---|---|
| Odds Ratio* [95% C.I.] | N | P Value | Odds Ratio [95% C.I.] | N | P Value | ||
| Indoor Smoking | Activity Limitations | 2.56 [1.21, 5.40] |
162 (539 forms) | 0.014 | 1.03 [0.18, 5.88] |
81 (274 forms) | 0.98 |
| Nighttime Symptoms | 2.27 [0.96, 5.38] |
162 (563 forms) | 0.06 | 2.83 [0.62, 12.85] |
81 (283 forms) | 0.18 | |
Odds ratios for respiratory outcomes (dependent variable) given reported indoor smoking (independent variable) were generated through logistic regression clustered by subject and adjusted for potential confounders, including race/ethnicity, insurance status, age at the time of environmental assessment, and age at the time of respiratory outcomes questionnaire completion.
Of the 244 subjects in this study, 162 reported no air purifier in the home, 81 reported having one, and 1 subject was missing this data.
Table 6.
Presence of Air Purifiers as a Modifier of Selected Respiratory Outcomes for Subjects on Respiratory Support
| No Air Purifier | Air Purifier | ||||||
|---|---|---|---|---|---|---|---|
| Odds Ratio* [95% C.I.] | N | P Value | Odds Ratio [95% C.I.] | N | P Value | ||
| Indoor Smoking | Cough or Wheeze | 2.35 [0.91, 6.07] |
82 (307 forms) | 0.08 | 2.98 [0.61, 14.62] |
32 (139 forms) | 0.18 |
| Activity Limitations | 3.67 [1.29, 10.41] |
82 (292 forms) | 0.015 | 5.06 [0.69, 36.87] |
32 (135 forms) | 0.11 | |
| Nighttime Symptoms | 6.85 [1.79, 26.17] |
82 (303 forms) | 0.005 | 6.10 [1.02, 36.50] |
32 (141 forms) | 0.047 | |
| Indoor Combustion | Inpatient Hospitalization | 3.18 [0.61, 16.46] |
82 (5305 forms) | 0.17 | All subjects reporting combustion were hospitalized | ||
Odds ratios for respiratory outcomes (dependent variable) given reported indoor smoking (independent variable) were generated through logistic regression clustered by subject and adjusted for potential confounders, including race/ethnicity, insurance status, age at the time of environmental assessment, and age at the time of respiratory outcomes questionnaire completion. Odds ratios for respiratory outcomes (dependent variable) given reported indoor combustion (independent variable) were generated through logistic regression clustered by subject and adjusted for potential confounders, including log of median household income, age at the time of environmental assessment, and age at the time of respiratory outcomes questionnaire completion.
Of the 244 subjects in this study, 162 reported no air purifier in the home, 81 reported having one, and 1 subject was missing this data. Of the 244 subjects in this study, 98 were on supplemental oxygen via nasal cannula, 15 were on home ventilators, and 1 had a tracheostomy without ventilator or oxygen use. Odds ratios were calculated in a similar manner to the all subjects regressions.
Oxygen Weaning:
To assess whether sources of indoor air pollution were associated with length of time on home supplemental oxygen, Kaplan-Meier methodology was employed. Of the 98 subjects discharged to home on supplemental oxygen via nasal cannula, 85 were weaned off of supplemental oxygen during follow-up; censored data were used for the remaining 13. The median time from NICU discharge to weaning from oxygen was 5.8 months (IQR: 3.0, 12.4). No differences in length of time to oxygen weaning were observed with either indoor smoking (log rank p=0.53) or indoor combustion (log rank p=0.76).
DISCUSSION
Our study found that most (76%) of infants were exposed to at least one combustible source of air pollution in the home (primarily gas stoves and heat). Exposure to any combustible source of indoor air pollution was associated with increased risk of hospitalization in infants and children on home respiratory support. Although only 14% of the study population reported a smoker residing in the home, we found that SHS exposure was associated with chronic respiratory symptoms, including activity limitation and nocturnal symptoms. Infants on respiratory support additionally had increased daytime cough and wheezing. There was no association between air pollution exposure in the home and the duration of supplemental oxygen use at home.
These findings are significant because there are currently no targeted long-term therapies for treating BPD and therefore management is focused on supportive respiratory care, reducing further lung injury, and optimizing nutrition in order to encourage lung growth.(16) Identification of modifiable risk factors is important, because intervention during this critical time of growth and development may lead to improved outcomes in respiratory health and lung function. Our results suggest that the impact may be even greater for the highest risk infants on respiratory support as reducing air pollution exposure in the home may reduce expensive hospitalizations.
The limited data available regarding the effects of SHS and other sources of indoor air pollution exposure in premature infants are mixed. Several authors, including a previous study in this cohort, have found that SHS exposure is associated with respiratory illnesses requiring acute care, recurrent wheezing, and activity limitation(12, 17) but a few have not corroborated these results. Martinez et al found that despite high exposure to SHS in a population of infants with BPD living in France, exposure was not associated with diagnosis of asthma, need for asthma medication, supplemental oxygen use, or hospitalizations for respiratory illness in the first two years of life. Because smoke exposure was based on parental report, this may have underestimated the number of children truly exposed.(18) In a 2014 sample of our registry population, we found that respiratory outcomes were not associated with SHS exposure. The survey used in that study may have underestimated the number of exposed participants because parents were asked, “Is there a smoker living in your home?” In our updated questionnaire, we asked whether smoking occurred inside the home or inside a shared building (e.g., apartment building) within the past 3 months as children not living with smokers in multiunit housing have higher nicotine metabolite levels than those living in detached homes.(19) The 2014 study also noted that infants who were exposed to SHS were more likely to be on inhaled corticosteroids which may have mitigated their symptoms.(20)
In a study that evaluated combustible sources of indoor air pollution on the respiratory health in very low birth weight infants, authors reported that living with a smoker and exposure to pests was associated with increased acute care visits but having a wood stove was not.(21) Other infant cohorts evaluating the association of indoor NO2 exposure and early life respiratory symptoms also found negative results.(22, 23) In a 2013 meta-analysis, the authors concluded that indoor NO2 exposure was associated with current wheeze, and gas cooking increased the risk of asthma. Only 4 of the 41 included studies were completed in infants, the remainder were in school aged children with and without asthma.(24) There are fewer studies measuring indoor PM2.5 in infant populations, but Hunt et al demonstrated that in a full-term infant cohort at risk for asthma, PM2.5 levels > 15 μm/m3 were associated with increased risk of wheezing during the first year of life.(25)
In terms of potential mitigation of indoor air pollution, about a third of the study population reported having an air purifier in their home. In a previous study investigating household activities associated with particulate matter concentrations in the homes of 300 children with asthma in Baltimore, only 1% of the study population reported using an air purifier.(26) In our study, the presence of an air purifier attenuated the effect of SHS exposure on reported activity limitation. The use of a HEPA (high-efficiency particulate air) indoor air purifier has been shown to be effective in reducing indoor air pollution resulting in decreased asthma symptoms(27) and so this may be an intervention to study further in homes of high risk infants with chronic lung disease.
Our study is limited by the fact that parents may underreport their child’s exposure to SHS and our unvalidated home characteristics questionnaire may not accurately predict levels of indoor particulate matter as it does not quantify gas stove, fireplace, exhaust fan, or air purifier use. In this study, only 14% of caretakers reported smoking in the home. A previous study in this registry population found that 20–28% of parents reported smoking in the home but in a follow up study, hair nicotine analysis found that almost 50% of participants may have been misclassified when relying on parent questionnaire.(12, 20) It also may be necessary in future survey design to include a question about a child’s known exposure to SHS outside the home.(28) We also did not collect any data on in utero smoking exposures, or distinguish between secondhand and thirdhand exposures, which may impact outcomes.
In summary, we have shown that combustible sources of indoor air pollution (such as gas stoves, fireplaces, and tobacco smoke exposure) were associated with increased respiratory morbidity in a group of high risk of infants born prematurely with BPD. Our data would suggest that the use of an air purifier may attenuate some of the adverse effects of SHS exposure. Our results support that indoor air pollution is a somewhat modifiable risk factor for respiratory health in infants with BPD. Future research should consider measuring indoor air pollution and SHS exposure directly because parent reported exposures may lead to misclassification bias. Air purifiers may be a method for reducing indoor air pollution short of eliminating exposure sources, but clinical trials are needed to evaluate the clinical impact of this intervention.
Figure 1.
Kaplan Meier plot depicting age of weaning off nasal cannula oxygen by reported indoor smoking status within the past 3 months.
Figure 2.
Kaplan Meier plot depicting age of weaning off nasal cannula oxygen by reported indoor combustion exposure status.
ACKNOWLEDGMENTS
We thank the families who participated in this study.
Funded by the American Academy of Pediatrics Julius B. Richmond Center of Excellence, the Flight Attendant Medical Research Institute, and the National Institutes of Health (1K23 ES029985-01[to J.R.] and R01 HL114800 [to S.M.]). The authors declare no conflicts of interest.
Abbreviations:
- BPD
bronchopulmonary dysplasia
- PM2.5
fine particulate matter
- NO2
nitrogen dioxide
Footnotes
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