Dataset Information

The Effect of Particulate Matter Reduction by Indoor Air Filter Use on Respiratory Symptoms and Lung Function: A Systematic Review and Meta-analysis.

ABSTRACT:

Purpose

Exposure to particulate matter (PM) is a key public health issue, but effective intervention has not yet been established. A systematic literature review and meta-analysis has been conducted to assess the relationship between the use of air filters, one of the most commonly studied interventions, and respiratory outcomes in patients with chronic respiratory diseases.

Methods

We systematically reviewed intervention studies on PM using PubMed, EMBASE, and Cochrane databases up to September 2019. Studies that included data on PM concentration changes and respiratory symptoms or lung function in patients with respiratory diseases were eligible for inclusion. Effect estimates were quantified separately using the random-effects model.

Results

Six studies were included in the quantitative analysis. Air filter use reduced indoor PM2.5 by 11.45 µg/m³ (95% confidence interval [CI], 6.88, 16.01 µg/m³). Air filter use was not associated with improvements in respiratory symptoms in 5 of the 6 studies or significant changes in the predicted forced expiratory volume in one second (FEV1) (mean change, -1.77%; 95% CI, -8.25%, 4.71%). Air filter use was associated with improved peak expiratory flow rate by 5.86 (95% CI, 3.5, 8.19 of standardized difference).

Conclusions

The findings of this systematic review suggest that air filters may reduce indoor PM and increase peak expiratory rate in asthmatic patients. However, most studies showed no significant effects of air filters on respiratory symptoms or FEV1. Further studies in regions with high-density PM may provide additional information on this issue.

Trial registration

PROSPERO Identifier: CRD42020156258.

SUBMITTER: Park HJ

PROVIDER: S-EPMC8419638 | biostudies-literature |

REPOSITORIES: biostudies-literature

ACCESS DATA

Similar Datasets

Project description:People generally spend more time indoors than outdoors resulting in a higher proportion of exposure to particulate matter (PM) occurring indoors. Consequently, indoor PM levels, in contrast to outdoor PM levels, may have a stronger relationship with lung function. To test this hypothesis, indoor and outdoor PM2.5 and fungal spore data were simultaneously collected from the homes of forty-four asthmatic children aged 10-16?years. An optical absorption technique was utilized on the collected PM2.5 mass to obtain concentrations of black carbon (BC) and ultraviolet light absorbing particulate matter, (UVPM; a marker of light absorbing PM2.5 emitted from smoldering organics). Enrolled children completed spirometry after environmental measurements were made. Given the high correlation between PM2.5, BC, and UVPM, principal component analysis was used to obtain uncorrelated summaries of the measured PM. Separate linear mixed-effect models were developed to estimate the association between principal components of the PM variables and spirometry values, as well as the uncorrelated original PM variables and spirometry values. A one-unit increase in the first principal component variable representing indoor PM (predominantly composed of UVPM and PM2.5) was associated with 4.1% decrease (99% CI?=?-6.9, -1.4) in FEV1/FVC ratio. 11.3??g/m3 increase in indoor UVPM was associated with 6.4% and 14.7% decrease (99% CI?=?-10.4, -2.4 and 99% CI?=?-26.3, -2.9, respectively) in percent predicted FEV1/FVC ratio and FEF25-75 respectively. Additionally, 17.7??g/m3 increase in indoor PM2.5 was associated with 6.1% and 12.9% decrease (99% CI?=?-10.2, -1.9 and 99% CI?=?-24.9, -1.0, respectively) in percent predicted FEV1/FVC ratio and FEF25-75, respectively. Outdoor PM, indoor BC, and indoor fungal spores were not significantly associated with lung function. The results indicate that indoor PM is more strongly associated with lung function in children with asthma as compared with outdoor PM.

Project description:Background - Multiple health effects are associated with moisture damage in buildings. Studies explaining these associations and cell-level mechanisms behind the observed health effects are urgently called for. Objectives - Alongside general toxicological markers, we focused on characterizing gene expression in human airway epithelium after exposure to indoor air particulate matter (PM) sampled from houses with and without moisture damage. Methods - We performed detailed technical building inspections in 25 residential houses and categorized them based on the detection of moisture damages and the probability of occupant exposure. PM sampling was complemented by microbiological and volatile organic compound assessment. We exposed airway constructs to three doses (1:16, 1:8, 1:4) of PM from moisture-damaged (index) and non-moisture-damaged (reference) houses. The RNA of exposed constructs was sequenced targeting toxicology -related genes. We did groupwise comparisons between index and reference houses and pairwise comparisons in matched index/reference houses. We analyzed general toxicological markers and imaged the constructs with electron microscopy. Results - In pairwise comparison, several genes were differentially expressed. Genes related to multiple toxicological pathways were highlighted, while none of the genes was consistently expressed in all the comparisons. In groupwise comparison, CYP1A1 was statistically significantly over-expressed in index houses at all doses (dose 1:16 log2FC = 0.007, padj = 0.03; dose 1:8 log2FC = 0.077, padj = 0.018; dose 1:4 log2FC = 0.270, padj = 0.002) and NFKB1 at the highest dose 1:4 (log2FC = 0.124, padj = 0.029). General toxicological markers did not separate the index/reference houses. Discussion - The exposure to PM from index houses activates toxicology -related genes in airway constructs. While differential expression was not consistent among all the index/reference pairs, possibly due to compositional differences of bioactive particles, our study highlights CYP1A1 and NFKB1 as potential targets in moisture damage -associated cellular responses.