Air pollution and lung function in children Garcia, Erika; Rice, Mary B.; Gold, Diane R.
Journal of allergy and clinical immunology,
07/2021, Letnik:
148, Številka:
1
Journal Article
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In this narrative review, we summarize the literature and provide updates on recent studies of air pollution exposures and child lung function and lung function growth. We include exposures to ...outdoor air pollutants that are monitored and regulated through air quality standards, and air pollutants that are not routinely monitored or directly regulated, including wildfires, indoor biomass and coal burning, gas and wood stove use, and volatile organic compounds. Included is a more systematic review of the recent literature on long-term air pollution and child lung function because this is an indicator of future adult respiratory health and exposure assessment tools have improved dramatically in recent years. We present “summary observations” and “knowledge gaps.” We end by discussing what is known about what can be done at the individual/household, local/regional, and national levels to overcome structural impediments, reduce air pollution exposures, and improve child lung function. We found a large literature on adverse air pollution effects on children’s lung function level and growth; however, many questions remain. Important areas needing further research include whether early-life effects are fixed or reversible; and what are windows of increased susceptibility, long-term effects of repeated wildfire events, and effects of air quality interventions.
Few studies have examined associations between long-term exposure to fine particulate matter (PM2.5) and lung function decline in adults.
To determine if exposure to traffic and PM2.5 is associated ...with longitudinal changes in lung function in a population-based cohort in the Northeastern United States, where pollution levels are relatively low.
FEV1 and FVC were measured up to two times between 1995 and 2011 among 6,339 participants of the Framingham Offspring or Third Generation studies. We tested associations between residential proximity to a major roadway and PM2.5 exposure in 2001 (estimated by a land-use model using satellite measurements of aerosol optical thickness) and lung function. We examined differences in average lung function using mixed-effects models and differences in lung function decline using linear regression models. Current smokers were excluded. Models were adjusted for age, sex, height, weight, pack-years, socioeconomic status indicators, cohort, time, season, and weather.
Living less than 100 m from a major roadway was associated with a 23.2 ml (95% confidence interval CI, -44.4 to -1.9) lower FEV1 and a 5.0 ml/yr (95% CI, -9.0 to -0.9) faster decline in FEV1 compared with more than 400 m. Each 2 μg/m(3) increase in average of PM2.5 was associated with a 13.5 ml (95% CI, -26.6 to -0.3) lower FEV1 and a 2.1 ml/yr (95% CI, -4.1 to -0.2) faster decline in FEV1. There were similar associations with FVC. Associations with FEV1/FVC ratio were weak or absent.
Long-term exposure to traffic and PM2.5, at relatively low levels, was associated with lower FEV1 and FVC and an accelerated rate of lung function decline.
Chen and Rice discuss a study by Bourbeau et al which examined dysanapsis, a mismatch of airway tree caliber to lung parenchyma size, as a potential indicator of pollution susceptibility, building on ...emerging evidence implicating airway abnormalities and impaired lung growth as chronic obstructive pulmonary disease (COPD) risk factors. In the study, long-term pollution exposure was associated with lower lung function at amounts within current air quality guidelines in Canada and the US but above the latest World Health Organization air quality guidelines. It suggests that adults with small airways relative to lung size may experience greater respiratory effects in association with long-term exposure to particulate matter pollution.
Although air pollution is well known to be harmful to the lung and airways, it can also damage most other organ systems of the body. It is estimated that about 500,000 lung cancer deaths and 1.6 ...million COPD deaths can be attributed to air pollution, but air pollution may also account for 19% of all cardiovascular deaths and 21% of all stroke deaths. Air pollution has been linked to other malignancies, such as bladder cancer and childhood leukemia. Lung development in childhood is stymied with exposure to air pollutants, and poor lung development in children predicts lung impairment in adults. Air pollution is associated with reduced cognitive function and increased risk of dementia. Particulate matter in the air (particulate matter with an aerodynamic diameter < 2.5 μm) is associated with delayed psychomotor development and lower child intelligence. Studies link air pollution with diabetes mellitus prevalence, morbidity, and mortality. Pollution affects the immune system and is associated with allergic rhinitis, allergic sensitization, and autoimmunity. It is also associated with osteoporosis and bone fractures, conjunctivitis, dry eye disease, blepharitis, inflammatory bowel disease, increased intravascular coagulation, and decreased glomerular filtration rate. Atopic and urticarial skin disease, acne, and skin aging are linked to air pollution. Air pollution is controllable and, therefore, many of these adverse health effects can be prevented.
Air pollution poses a great environmental risk to health. Outdoor fine particulate matter (particulate matter with an aerodynamic diameter < 2.5 μm) exposure is the fifth leading risk factor for ...death in the world, accounting for 4.2 million deaths and > 103 million disability-adjusted life years lost according to the Global Burden of Disease Report. The World Health Organization attributes 3.8 million additional deaths to indoor air pollution. Air pollution can harm acutely, usually manifested by respiratory or cardiac symptoms, as well as chronically, potentially affecting every organ in the body. It can cause, complicate, or exacerbate many adverse health conditions. Tissue damage may result directly from pollutant toxicity because fine and ultrafine particles can gain access to organs, or indirectly through systemic inflammatory processes. Susceptibility is partly under genetic and epigenetic regulation. Although air pollution affects people of all regions, ages, and social groups, it is likely to cause greater illness in those with heavy exposure and greater susceptibility. Persons are more vulnerable to air pollution if they have other illnesses or less social support. Harmful effects occur on a continuum of dosage and even at levels below air quality standards previously considered to be safe.
Garcia and Rice discuss the population-based study by Shin and colleagues of all 5 million adults living in the Canadian province of Ontario who were free of asthma or COPD diagnosis in 2001. During ...the 15-year study follow-up period, over 340,000 incident cases of COPD and over 218,000 incident cases of asthma were identified. Using a 3-year average of air pollution exposure with a 1-year lag, the authors found that multiple outdoor pollutants, including fine particulate matter, nitrogen dioxide, and ozone, were associated with greater COPD incidence, which is defined as a COPD hospitalization or at least three physician claims for COPD within 2 years. In contrast, there were no associations between exposure to these pollutants and new adult-onset asthma.
"Candidatus Berkiella cookevillensis" (strain CC99) and "Candidatus Berkiella aquae" (strain HT99), belonging to the Coxiellaceae family, are gram-negative bacteria isolated from amoebae in biofilms ...present in human-constructed water systems. Both bacteria are obligately intracellular, requiring host cells for growth and replication. The intracellular bacteria-containing vacuoles of both bacteria closely associate with or enter the nuclei of their host cells. In this study, we analyzed the genome sequences of CC99 and HT99 to better understand their biology and intracellular lifestyles. The CC99 genome has a size of 2.9Mb (37.9% GC) and contains 2,651 protein-encoding genes (PEGs) while the HT99 genome has a size of 3.6Mb (39.4% GC) and contains 3,238 PEGs. Both bacteria encode high proportions of hypothetical proteins (CC99: 46.5%; HT99: 51.3%). The central metabolic pathways of both bacteria appear largely intact. Genes for enzymes involved in the glycolytic pathway, the non-oxidative branch of the phosphate pathway, the tricarboxylic acid pathway, and the respiratory chain were present. Both bacteria, however, are missing genes for the synthesis of several amino acids, suggesting reliance on their host for amino acids and intermediates. Genes for type I and type IV (dot/icm) secretion systems as well as type IV pili were identified in both bacteria. Moreover, both bacteria contain genes encoding large numbers of putative effector proteins, including several with eukaryotic-like domains such as, ankyrin repeats, tetratricopeptide repeats, and leucine-rich repeats, characteristic of other intracellular bacteria.
Studies of air pollution exposure and arterial stiffness have reported inconsistent results and large studies employing the reference standard of arterial stiffness, carotid-femoral pulse-wave ...velocity (CFPWV), have not been conducted.
To study long-term exposure to ambient fine particles (PM2.5), proximity to roadway, and short-term air pollution exposures in relation to multiple measures of arterial stiffness in the Framingham Heart Study.
We assessed central arterial stiffness using CFPWV, forward pressure wave amplitude, mean arterial pressure and augmentation index. We investigated long-and short-term air pollution exposure associations with arterial stiffness with linear regressions using long-term residential PM2.5 (2003 average from a spatiotemporal model using satellite data) and proximity to roadway in addition to short-term averages of PM2.5, black carbon, particle number, sulfate, nitrogen oxides, and ozone from stationary monitors.
We examined 5842 participants (mean age 51 ± 16, 54% women). Living closer to a major roadway was associated with higher arterial stiffness (0.11 m/s higher CFPWV 95% CI: 0.01, 0.22 living <50 m vs 400 ≤ 1000 m). We did not observe association between arterial stiffness measures and long-term PM2.5 or short-term levels of PM2.5, particle number, sulfate or ozone. Higher levels of black carbon and nitrogen oxides in the previous days were unexpectedly associated with lower arterial stiffness.
Long-term exposure to PM2.5 was not associated with arterial stiffness but positive associations with living close to a major road may suggest that pollutant mixtures very nearby major roads, rather than PM2.5, may affect arterial stiffness. Furthermore, short-term air pollution exposures were not associated with higher arterial stiffness.
•Living nearby a major road was associated with higher arterial stiffness.•Particle matter measured by satellite was not associated with arterial stiffness.•No associations were observed for short-term exposure to air pollution.
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