Introduction: Indoor nitrogen dioxide (NO2) sources include gas heating, cooking, and infiltration from outdoors. Associations with pulmonary function, systemic inflammation, and oxidative stress in patients with chronic obstructive pulmonary disease (COPD) are uncertain.
Methods: We recruited 144 COPD patients at the VA Boston Healthcare System between 2012 and 2017. In-home NO2 was measured using an Ogawa passive sampling badge for a week seasonally followed by measuring plasma biomarkers of systemic inflammation (C-reactive protein [CRP] and interleukin-6 [IL-6]), urinary oxidative stress biomarkers (8-hydroxy-2'deoxyguanosine [8-OHdG] and malondialdehyde [MDA]), and pre- and postbronchodilator spirometry. Linear mixed effects regression with a random intercept for each subject was used to assess associations with weekly NO2. Effect modification by COPD severity and by body mass index (BMI) was examined using multiplicative interaction terms and stratum-specific effect estimates.
Results: Median (25%ile, 75%ile) concentration of indoor NO2 was 6.8 (4.4, 11.2) ppb. There were no associations observed between NO2 with CRP, 8-OHdG, or MDA. Although the confidence intervals were wide, there was a reduction in prebronchodilator FEV1 and FVC among participants with more severe COPD (FEV1: -17.36 mL; -58.35, 23.60 and FVC: -28.22 mL; -91.49, 35.07) that was greater than in patients with less severe COPD (FEV1: -1.64 mL; -24.80, 21.57 and FVC: -6.22 mL; -42.16, 29.71). In participants with a BMI <30, there was a reduction in FEV1 and FVC.
Conclusions: Low-level indoor NO2 was not associated with systemic inflammation or oxidative stress. There was a suggestive association with reduced lung function among patients with more severe COPD and among patients with a lower BMI.
Background: Heat effects on respiratory mortality are known, mostly from time-series studies of city-wide data. A limited number of studies have been conducted at the national level or covering non-urban areas. Effect modification by area-level factors has not been extensively investigated. Our study assessed the heat effects on respiratory mortality at a small administrative area level in Norway, Germany, and England and Wales, in the warm period (May-September) within 1996-2018. Also, we examined possible effect modification by several area-level characteristics in the framework of the EU-Horizon2020 EXHAUSTION project.
Methods: Daily respiratory mortality counts and modeled air temperature data were collected for Norway, Germany, and England and Wales at a small administrative area level. The temperature-mortality association was assessed by small area-specific Poisson regression allowing for overdispersion, using distributed lag non-linear models. Estimates were pooled at the national level and overall using a random-effect meta-analysis. Age- and sex-specific models were also applied. A multilevel random-effects model was applied to investigate the modification of the heat effects by area-level factors.
Results: A rise in temperature from the 75th to 99th percentile was associated with a 27% (95% confidence interval [CI] = 19%, 34%) increase in respiratory mortality, with higher effects for females. Increased population density and PM2.5 concentrations were associated with stronger heat effects on mortality.
Conclusions: Our study strengthens the evidence of adverse heat effects on respiratory mortality in Northern Europe by identifying vulnerable subgroups and subregions. This may contribute to the development of targeted policies for adaptation to climate change.
[This corrects the article DOI: 10.1097/EE9.0000000000000265.].
Background: Nonalcoholic fatty liver disease (NAFLD) is a disease characterized by lipid accumulation within hepatocytes, ranging from simple steatosis to steatohepatitis, in the absence of secondary causes of hepatic fat accumulation. Although air pollution (AP) has been associated with several conditions related to NAFLD (e.g., metabolic syndrome, type 2 diabetes mellitus), few studies have explored an association between AP and NAFLD. The aim of the study was to investigate whether exposure to AP is associated with NAFLD prevalence.
Methods: We used baseline cross-sectional data (2000-2003) of the Heinz-Nixdorf-Recall cohort study in Germany (baseline n = 4,814), a prospective population-based cohort study in the urbanized Ruhr Area. Mean annual exposure to size-fractioned particulate matter (PM10, PM2.5, PMcoarse, and PM2.5abs), nitrogen dioxide, and particle number was assessed using two different exposure models: a chemistry transport dispersion model, which captures urban background AP exposure on a 1 km2 grid at participant's residential addresses, and a land use regression model, which captures point-specific AP exposure at participant's residential addresses. NAFLD was assessed with the fatty liver index (n = 4,065), with NAFLD defined as fatty liver index ≥60. We estimated ORs of NAFLD per interquartile range of exposure using logistic regression, adjusted for socio-demographic and lifestyle variables.
Results: We observed a NAFLD prevalence of 31.7% (n = 1,288). All air pollutants were positively associated with NAFLD prevalence, with an OR per interquartile range for PM2.5 of 1.11 (95% confidence interval [CI] = 1.00, 1.24) using chemistry transport model, and 1.06 (95% CI = 0.94, 1.19) using the land use regression model, respectively.
Conclusion: There was a positive association between long-term AP exposure and NAFLD.
Rationale: The prevalence of nontuberculous mycobacterial (NTM) pulmonary disease varies geographically in the United States. Previous studies indicate that the presence of certain water-quality constituents in source water increases NTM infection risk.
Objective: To identify water-quality constituents that influence the risk of NTM pulmonary infection in persons with cystic fibrosis in the United States.
Methods: We conducted a population-based case-control study using NTM incidence data collected from the Cystic Fibrosis Foundation Patient Registry during 2010-2019. We linked patient zip code to the county and associated patient county of residence with surface water data extracted from the Water Quality Portal. We used logistic regression models to estimate the odds of NTM infection as a function of water-quality constituents. We modeled two outcomes: pulmonary infection due to Mycobacterium avium complex (MAC) and Mycobacterium abscessus species.
Results: We identified 484 MAC cases, 222 M. abscessus cases and 2816 NTM-negative cystic fibrosis controls resident in 11 states. In multivariable models, we found that for every 1-standardized unit increase in the log concentration of sulfate and vanadium in surface water at the county level, the odds of infection increased by 39% and 21%, respectively, among persons with cystic fibrosis with MAC compared with cystic fibrosis-NTM-negative controls. When modeling M. abscessus as the dependent variable, every 1-standardized unit increase in the log concentration of molybdenum increased the odds of infection by 36%.
Conclusions: These findings suggest that naturally occurring and anthropogenic water-quality constituents may influence the NTM abundance in water sources that supply municipal water systems, thereby increasing MAC and M. abscessus infection risk.
Background: Past research on the impact of climatic events, such as drought, on birth outcomes has primarily been focused in Africa, with less research in South Asia, including Nepal. Existing evidence has generally found that drought impacts birthweight and infant sex, with differences by trimester. Additionally, less research has looked at the impact of excess rain on birth outcomes or focused on the impact of rainfall extremes in the preconception period. Using data from a large demographic surveillance system in Nepal, combined with a novel measure of drought/excess rainfall, we explore the impact of these on birthweight by time in pregnancy.
Methods: Using survey data from the 2016 to 2019 Chitwan Valley Study in rural Nepal combined with data from Climate Hazards InfraRed Precipitation with Station, we explored the association between excess rainfall and drought and birthweight, looking at exposure in the preconception period, and by trimester of pregnancy. We also explore the impact of excess rainfall and drought on infant sex and delivery with a skilled birth attendant. We used multilevel regressions and explored for effect modification by maternal age.
Results: Drought in the first trimester is associated with lower birthweight (β = -82.9 g; 95% confidence interval [CI] = 164.7, -1.2) and drought in the preconception period with a high likelihood of having a male (odds ratio [OR] = 1.41; 95% CI = 1.01, 2.01). Excess rainfall in the first trimester is associated with high birthweight (β = 111.6 g; 95% CI = 20.5, 202.7) and higher odds of having a male (OR = 1.48; 95% CI = 1.02, 2.16), and in the third trimester with higher odds of low birth weight (OR = 2.50; 95% CI = 1.40, 4.45).
Conclusions: Increasing rainfall extremes will likely impact birth outcomes and could have implications for sex ratios at birth.
Epidemiologic evidence on the relationships between air pollution and the risks of primary cancers other than lung cancer remained largely lacking. We aimed to examine associations of 10-year exposures to fine particulate matter (PM2.5) and nitrogen dioxide (NO2) with risks of breast, prostate, colorectal, and endometrial cancers.
Methods: For each cancer, we constructed a separate cohort among the national Medicare beneficiaries during 2000 to 2016. We simultaneously examined the additive associations of six exposures, namely, moving average exposures to PM2.5 and NO2 over the year of diagnosis and previous 2 years, previous 3 to 5 years, and previous 6 to 10 years, with the risk of first cancer diagnosis after 10 years of follow-up, during which there was no cancer diagnosis.
Results: The cohorts included 2.2 to 6.5 million subjects for different cancers. Exposures to PM2.5 and NO2 were associated with increased risks of colorectal and prostate cancers but were not associated with endometrial cancer risk. NO2 was associated with a decreased risk of breast cancer, while the association for PM2.5 remained inconclusive. At exposure levels below the newly updated World Health Organization Air Quality Guideline, we observed substantially larger associations between most exposures and the risks of all cancers, which were translated to hundreds to thousands new cancer cases per year within the cohort per unit increase in each exposure.
Conclusions: These findings suggested substantial cancer burden was associated with exposures to PM2.5 and NO2, emphasizing the urgent need for strategies to mitigate air pollution levels.
Per- and polyfluoroalkyl substances (PFAS) are persistent environmental contaminants that induce immunotoxicity in experimental studies; however, epidemiological evidence-particularly during pregnancy-is scarce. We quantified associations between first trimester plasma perfluorooctanoic acid (PFOA), perfluorooctane sulfonate (PFOS), and perfluorohexane sulfonate (PFHxS) concentrations and third trimester concentrations of inflammatory biomarkers and determined if these associations were modified by fetal sex.
Methods: We analyzed data from 1411 participants, recruited between 2008 and 2011, in the Maternal-Infant Research on Environmental Chemicals study. Our primary outcome was a composite inflammatory index derived by summing the z-scores of eight proinflammatory biomarkers. Using multivariable linear regression models, we quantified associations between each PFAS and the inflammatory index and individual biomarkers. We quantified the effects of the PFAS mixture using weighted quantile sum regression, and evaluated effect modification using product terms and sex-stratified models.
Results: Each doubling of PFOA and PFHxS was associated with a 0.38 (95% CI, 0.09, 0.67) and 0.21 (95% CI, 0.01, 0.41) SD increase in the proinflammatory index, respectively. A one-quartile increase in the PFAS mixture was associated with a 0.40 (95% CI, 0.09, 0.71) SD increase in the proinflammatory index. In individual models, we observed positive associations between PFAS and concentrations of monocyte chemoattractant protein-1, macrophage inflammatory protein-1β, and matrix metalloproteinases-9; however, the magnitude and precision varied according to the specific PFAS. Sex-specific findings were identified in few PFAS-biomarker associations.
Conclusions: PFOA, PFOS, and PFHxS, individually and as a mixture, were positively associated with proinflammatory biomarkers during pregnancy.
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