In response to the evidenced connection between pediatric asthma development and air pollution exposure, investigators have sought out association indicators as early as in utero.
Several epidemiological studies have sought to determine correlations between ambient air pollution and development of childhood asthma. Regional concentrations of environmental pollutants have been shown to have a statistically significant effect on childhood asthma morbidity.1 The most recently-published US Centers for Disease Control and Prevention (CDC) data show that asthma-related concerns accounted for 6.2% of all-age patient visits to office-based physicians, and 1.7 million visits to emergency departments in 2015. Mortality rates due to asthma were 3,615, about 1.1 deaths per 100,000 that year.
In 2016, 14.4% of boys and 11.0% of girls were told that they had asthma, and 9.3% of boys and 7.4% of girls were told by doctors that they still have asthma.2 Deeper examination of the data show that of children who still have asthma, 7.0% are white, 6.8% are Hispanic or Latino, 4.0% are Asian, while 15.9% are African-American and 16.1% are American Indian or Alaska Native. Poverty status also apparently plays a role in development of asthma, as asthma afflicted 11.7% of those with family income under $35,000/year, compared to 7.1% of those with family income over $35,000. Further breakdown of the statistics shows an inverse relationship of the percentage of children afflicted with asthma with family income level. There was a 9.2% rate associated with income levels of $35,000—$49,999, a 7.3% rate with incomes of $50,000–74,999, a 6.7% rate with incomes of $75,000–$99,999, and a 6.3% rate with incomes of $100,000 or more.
In response to growing recognition of the connection between the development of childhood asthma and exposure to air pollution, Clark et al hypothesized that a causal relationship exists between ambient air pollution in utero and during the first year of life, and subsequent risk of asthma development.3 To answer their hypothesis, the investigators utilized a population-based nested case—control study. They found significantly increased risks of asthma diagnosis correlated with early life exposure to the following airborne environmental toxins: carbon monoxide (CO), nitric oxide (NO), nitric dioxide (NO2), particulate matter ≤10 μm in aerodynamic diameter (PM10), sulfur dioxide (SO2), and black carbon. Traffic-related pollutants, (NO, NO2, CO, and black carbon) were associated with the highest risk estimate. Residence near industrial sites and exposure to PM10 and SO2 also accounted for elevated risk. The investigators acknowledge limitations in their study design that utilized simple proximity measures to identify cases of children with asthma diagnoses.
Several uncontrollable variables make decisive pinpointing asthma pathogenesis and exacerbations difficult. “I’m always somewhat reluctant to attribute asthma exacerbations to atmospheric pollution as a primary cause,” Neil Johnston, MSc, assistant professor, division of respirology, department of medicine at McMaster University, and epidemiologist, Firestone Institute for Respiratory Health, told MD Magazine®. “Asthma exacerbations are usually multi-factorial and while the immediate trigger is frequently the presence of a viral infection, particularly of human rhinovirus, the presence of allergies, degree of compliance with control medication, access to quality medical care, home environment (eg, parental smoking) and yes, possibly ambient air quality, all may play a role. The degree to which these factors do play a role will be influenced by poverty and social inequity and unfortunately residential areas with high levels of air pollution tend to be those in which poor people live.”
The results of a study conducted by Kravitz-Wirtz and colleagues4 produced similar findings to that of the study done by Clark et al, finding that exposure to air pollution in early life may be associated with asthma development. The investigators examined connections between childhood asthma and air pollution exposure during prenatal and early postnatal periods. Their findings were consistent with that of prior research studies, in that they found associations between future asthma risk and future development of asthma. Based on their data, their analyses showed that children exposed to high concentrations of NO2 at early ages than children who were exposed to low concentrations of NO2.
Conducting the first study to assess absolute, rather than relative, changes in asthma risk, Pennington and colleagues undertook a large retrospective birth cohort study of children born between 2000 and 2010, the Kaiser Air Pollution and Pediatric Asthma (KAPPA) Study, to determine whether exposure to air pollution from mobile sources during pregnancy or the first year of life increased the risk of developing childhood asthma.5 Asthma was defined as at least 1 asthma diagnosis and 1 prescribed asthma medication (including both steroid and non-steroid asthma controllers and relievers). Rather than rely on parental-reported asthma data, the investigators utilized data obtained through medical records. Since early-onset asthma can often be transient, the team completed an additional analysis to determine whether asthma is associated with lasting asthma phenotypes. Children without evidence of asthma morbidity in the previous year were excluded from the analysis.
The study design, using the well-defined KAPPA cohort of 24,608 children, 23,100 of whom had estimates of air pollution during the first year of life and 19,951 of whom had estimates of prenatal exposure to air pollution, enabled the investigators to examine the higher proportion of African-American children, a group disproportionately affected by asthma. The study included 35% African-American children. Pennington and colleagues further analyzed relevant covariates: sex, race, ethnicity, maternal asthma, maternal age, parental education, maternal marital status, neighborhood socioeconomic status (SES), birth year, and city region. Data showing higher percentages of childhood asthma incidence in lower-income areas led the investigators to hypothesize that SES would be an important confounding variable. To control for SES, the investigators obtained demographic clusters to categorize census block groups into 18 categories that were characterized from low to high SES. Since urban areas are strongly associated with higher levels of air pollutant concentrations, the variable was included in models to resolve concerns about residential confounding by SES.
To estimate air pollution data in longitudinal fashion to account for traffic patterns, particle composition, and meteorology and utilize data from stationary air pollution monitors for calibration, Pennington and colleagues estimated airborne pollution exposure (PM2.5, NO, NO2, and CO) using prospectively collected residential locations of mothers and their children. Annual average estimates for PM2.5, NO, NO2, and CO were collected for the years 2002-2011 at 250-meter resolution using a Research LINE-source dispersion model for near-surface releases (RLINE).
Of the analyzed covariates, the investigators found that the strongest predictors of childhood asthma were maternal asthma, male sex, and black race. The strongest determinant of residential exposure to air pollution was proximity to city center, with an inverse relationship of magnitude of exposure to increasing distance from city center. A key finding was that exposure distributions were similar between African-American and white children. Ethnicity, maternal age, parental education, and maternal marital status were not significant and were dropped from adjusted models. The investigators acknowledged several limitations of their study, including high drop-out rate of subjects and medical records reflecting inherent difficulties in early-life asthma diagnoses. Nonetheless, a surprising finding was a negative association between mobile source of air pollution and asthma; descriptive analyses showed a strong spatial pattern in their data, that increasing distance from the city center was correlated with increasing asthma rates and decreasing pollution.
The authors offered a potential explanation, that other factors change with increasing distance from city center, for example, access to health care resources and utilization rate. In their recently-published study, “Home Medication Readiness for Preschool Children with Asthma,” Callaghan-Koru and colleagues found that only 79% of low-income urban preschoolers prescribed controller medication actually had it in their home.6 Their study participants included 288 preschoolers (mean age 4.2, standard deviation 0.7), 92% of whom were African-American. The investigators concluded that assessing medication readiness is an under-recognized barrier to adherence to medication protocol.
In Vital Signs: Asthma in Children — United States, 2001—2016, Zahran and colleagues found that despite the fact that more children with asthma received an asthma action plan and were taught how to recognize and respond to early signs of an asthma attack in 2013, less than half of children (46%) received advice on environmental control, indicating a need for further improvement in these areas.7