Early life exposure to fine particulate matter and childhood asthma in Beijing, China: A case-control study

Abstract Background Short-term exposure to ozone and nitrogen dioxide is a risk factor for acute exacerbation (AE) of idiopathic pulmonary fibrosis (AE-IPF). The comprehensive roles of exposure to fine particulate matter in AE-IPF remain unclear. We aim to investigate the association of short-term exposure to fine particulate matter with the incidence of AE-IPF and to determine the exposure-risk time window during 3 months before the diagnosis of AE-IPF. Methods IPF patients were retrospectively identified from the nationwide registry in Japan. We conducted a case–control study to assess the correlation between AE-IPF incidence and short-term exposure to eight air pollutants, including particulate matter < 2.5 µm (PM2.5). In the time-series data, we compared monthly mean exposure concentrations between months with AE (case months) and those without AE (control months). We used multilevel mixed-effects logistic regression models to consider individual and institutional-level variables, and also adjusted these models for several covariates, including temperature and humidity. An additional analysis with different monthly lag periods was conducted to determine the risk-exposure time window for 3 months before the diagnosis of AE-IPF. Results Overall, 152 patients with surgically diagnosed IPF were analyzed. AE-IPF was significantly associated with an increased mean exposure level of nitric oxide (NO) and PM2.5 30 days prior to AE diagnosis. Adjusted odds ratio (OR) with a 10 unit increase in NO was 1.46 [95% confidence interval (CI) 1.11–1.93], and PM2.5 was 2.56 (95% CI 1.27–5.15). Additional analysis revealed that AE-IPF was associated with exposure to NO during the lag periods lag 1, lag 2, lag 1–2, and lag 1–3, and PM2.5 during the lag periods lag 1 and lag 1–2. Conclusions Our results show that PM2.5 is a risk factor for AE-IPF, and the risk-exposure time window related to AE-IPF may lie within 1–2 months before the AE diagnosis. Further investigation is needed on the novel findings regarding the exposure to NO and AE-IPF.

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Test-retest reliability of a computer-assisted self-administered questionnaire on early life exposure in a nasopharyngeal carcinoma case-control study

Scientific Reports ◽

10.1038/s41598-018-25046-y ◽

2018 ◽

Vol 8 (1) ◽

Cited By ~ 1

Author(s):

Zhi-Ming Mai ◽

Jia-Huang Lin ◽

Shing-Chun Chiang ◽

Roger Kai-Cheong Ngan ◽

Dora Lai-Wan Kwong ◽

...

Keyword(s):

Nasopharyngeal Carcinoma ◽

Early Life ◽

Case Control Study ◽

Case Control ◽

Computer Assisted ◽

Retest Reliability ◽

Early Life Exposure ◽

Test Retest Reliability ◽

Self Administered Questionnaire ◽

Control Study

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In Utero and Early-Life Exposure to Ambient Air Toxics and Childhood Brain Tumors: A Population-Based Case–Control Study in California, USA

Environmental Health Perspectives ◽

10.1289/ehp.1408582 ◽

2016 ◽

Vol 124 (7) ◽

pp. 1093-1099 ◽

Cited By ~ 17

Author(s):

Ondine S. von Ehrenstein ◽

Julia E. Heck ◽

Andrew S. Park ◽

Myles Cockburn ◽

Loraine Escobedo ◽

...

Keyword(s):

Brain Tumors ◽

Early Life ◽

Case Control Study ◽

Ambient Air ◽

Population Based ◽

In Utero ◽

Case Control ◽

Childhood Brain Tumors ◽

Early Life Exposure ◽

Control Study

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Early life exposure to diagnostic radiation and ultrasound scans and risk of childhood cancer: case-control study

BMJ ◽

10.1136/bmj.d472 ◽

2011 ◽

Vol 342 (feb10 1) ◽

pp. d472-d472 ◽

Cited By ~ 70

Author(s):

P. Rajaraman ◽

J. Simpson ◽

G. Neta ◽

A. Berrington de Gonzalez ◽

P. Ansell ◽

...

Keyword(s):

Childhood Cancer ◽

Early Life ◽

Case Control Study ◽

Case Control ◽

Cancer Case ◽

Early Life Exposure ◽

Diagnostic Radiation ◽

Control Study

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Household mold exposure interacts with inflammation-related genetic variants on childhood asthma: a case–control study

BMC Pulmonary Medicine ◽

10.1186/s12890-021-01484-9 ◽

2021 ◽

Vol 21 (1) ◽

Author(s):

Yu Zhang ◽

Li Hua ◽

Quan-Hua Liu ◽

Shu-Yuan Chu ◽

Yue-Xin Gan ◽

...

Keyword(s):

Childhood Asthma ◽

Case Control Study ◽

Additive Model ◽

Case Control ◽

Nucleotide Polymorphisms ◽

Additive Interaction ◽

Asthmatic Children ◽

Gene Environment ◽

Mold Exposure ◽

Control Study

Abstract Background A number of studies have examined the association between mold exposure and childhood asthma. However, the conclusions were inconsistent, which might be partly attributable to the lack of consideration of gene function, especially the key genes affecting the pathogenesis of childhood asthma. Research on the interactions between genes and mold exposure on childhood asthma is still very limited. We therefore examined whether there is an interaction between inflammation-related genes and mold exposure on childhood asthma. Methods A case–control study with 645 asthmatic children and 910 non-asthmatic children aged 3–12 years old was conducted. Eight single nucleotide polymorphisms (SNPs) in inflammation-related genes were genotyped using MassARRAY assay. Mold exposure was defined as self-reported visible mold on the walls. Associations between visible mold exposure, SNPs and childhood asthma were evaluated using logistic regression models. In addition, crossover analyses were used to estimate the gene-environment interactions on childhood asthma on an additive scale. Results After excluding children without information on visible mold exposure or SNPs, 608 asthmatic and 839 non-asthmatic children were included in the analyses. Visible mold exposure was reported in 151 asthmatic (24.8%) and 119 non-asthmatic children (14.2%) (aOR 2.19, 95% CI 1.62–2.97). The rs7216389 SNP in gasdermin B gene (GSDMB) increased the risk of childhood asthma with each C to T substitution in a dose-dependent pattern (additive model, aOR 1.32, 95% CI 1.11–1.57). Children carrying the rs7216389 T allele and exposed to visible mold dramatically increased the risk of childhood asthma (aOR 3.21; 95% CI 1.77–5.99). The attributable proportion due to the interaction (AP: 0.47, 95% CI 0.03–0.90) and the relative excess risk due to the interaction (RERI: 1.49, 95% CI 0–2.99) were statistically significant. Conclusions In the present study, there was a significant additive interaction between visible mold exposure and rs7216389 SNP on childhood asthma. Future studies need to consider the gene-environment interactions when exploring the risk factors of childhood asthma.

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