Indoor air pollution from solid fuels and peripheral Blood DNA methylation: Findings from a population study in Warsaw, Poland
Introduction
Approximately half of the world׳s population uses solid fuels including coal, wood, dung, and crop residues for cooking or home heating (Torres-Duque et al., 2008). Usage distributions vary among countries with the largest prevalence in rural areas of developing countries, while a number of households in developed countries still use wood or other biomass products for heating (Naeher et al., 2007, Forum of International Respiratory Studies (FIRS) Task Force on Health Effects of Biomass Exposure, 2008). The fuels are typically burned inefficiently in open fires, leading to high emission rates and high levels of indoor air pollution (Lewtas, 2007, Forum of International Respiratory Studies (FIRS) Task Force on Health Effects of Biomass Exposure, 2008). Products of incomplete combustion contain particulate matter (PM), carbon monoxide, nitrogen and sulfur oxides, and many organic compounds such as carcinogens, e.g. (or including) polycyclic hydrocarbons (Lewtas, 2007, Forum of International Respiratory Studies (FIRS) Task Force on Health Effects of Biomass Exposure, 2008). In light of the high concentrations of the many pollutants, exposure to indoor air pollution presents a huge global public health concern (WHO International Agency for Research on Cancer Monograph Working Group, 2006, Naeher et al., 2007). The Global Burden of Disease project (GBD-2010) has estimated that household air pollution due to the use of solid cookfuels is responsible for about 3.9 million premature deaths each year, and about 4.8% of the global burden of disease (Smith et al., 2014). Based on evidence in both humans and experimental animals, exposure to indoor emissions from household combustion of coal has been concluded as a carcinogen to human, while biomass-smoke exposure (mainly wood) is a probable carcinogen to human (Straif et al., 2006). Although the amount of indoor air pollution exposure depends on the type of fuel used, the nature of the combustion, the location and the length of time exposed to polluted environment, women and children who are at home for most of the day are the most vulnerable (IARC, 2010). Further, there has been evidence linked to early-life (prenatal, infants, children and adolescents) periods exposure to air pollution with adulthood health effects in both animal and human studies (Soto-Martinez and Sly, 2010, Weldy et al., 2013). Although the underlying biological mechanisms are not clear, one possible mechanism is that there are epigenetic alterations resulting from these exposures, which play a role in the development of adverse health effects.
It is now widely acknowledged that epigenetic alterations can have various impacts on disease susceptibility and development. As an important mechanism of epigenetic changes, aberrant DNA methylation, including loss of genome-wide (global) methylation and site-specific hypermethylation, has been attributed to carcinogenesis and many other diseases (Baylin and Jones, 2011, Brennan and Flanagan, 2012). The level of DNA methylation is sensitive to various types of environmental exposures including benzene, arsenic, lead, persistent organic pollutants, as well as air pollutants, especially the exposures during early-life period (Bernal and Jirtle, 2010, Lambrou et al., 2012, Tang et al., 2012, Janssen et al., 2013). There is a large literature on DNA methylation alterations at the tissue level; more recently, peripheral blood DNA methylation changes in white blood cells have also been investigated as risk factor or potential cancer risk markers in some studies (Terry et al., 2011). However, data on how exposure to indoor air pollution both over the lifetime and during different periods of the lifetime is related to global methylation in blood DNA are still very limited.
Insulin-like growth factor 2 (IGF2) is one of two ligands within the genome׳s insulin network, and is necessary for the proper control of somatic growth, especially throughout early life (Werner and Le Roith, 2000, Livingstone, 2013). The IGF2/H19 gene locus is involved in early development through DNA methylation, and is one of the best studied imprinted genomic loci (Ollikainen and Craig, 2011). Genomic imprinting is a form of gene silencing that is regulated by gene-specific imprinting control regions (ICRs) through parent-of-origin differential methylation (Bell and Felsenfeld, 2000). Both animal models and human studies have shown that adverse prenatal environmental exposure is associated with subsequent IGF2 ICR methylation disruption (Wu et al., 2004, Heijmans et al., 2008), suggesting this may be an “environmental sensor” or biomarker of environment exposure. There are a few studies of the associations of early-life exposure to indoor air pollution with methylation of IGF2/H19 ICR in blood DNA from women.
To better understand the relationship of exposure to indoor air pollution from solid fuels at different lifetime periods with blood DNA methylation levels, we evaluated global DNA methylation and methylation levels of IGF2/H19 ICR in peripheral blood in population-based women who had never smoked cigarettes.
Section snippets
Study population
The study population was derived from the population-based controls of a case-control study of lung cancer conducted in Warsaw, Poland during 1998–2001. The population-based controls were randomly selected from the electronic registry of residents of Warsaw, Poland, and were frequency-matched to cases by age group (±3 years), geographic area, and gender. Details of the recruitment methods have been published elsewhere (Lissowska et al., 2005, Zeka et al., 2006). Interviews were completed for
Results
Table 1 summarizes selected characteristics of never-smoking women with DNA samples from Warsaw, Poland. Among them, 34 (80.9%) reported ever used any solid fuel at homes during their lifetime, with the mean lifetime duration of exposure of 27.0 years. The main solid fuel exposure type was coal, with 24 (57.1%) women having used coal and 7 (16.7%) having used both coal and wood during their lifetime. The mean level of LUMA methylation was 68.5% among 42 participants in the study population.
Discussion
To our knowledge, this is the first population-based study to access associations of exposure to indoor air pollution from solid fuels with global DNA methylation in peripheral blood. We found that ever exposure to indoor air pollution from solid fuel was associated with decreased levels of global methylation in peripheral blood among never-smoking women. Similarly, using both coal and wood for heating or cooking before age 20 was associated with reduction in global DNA methylation. Our
Conflict of interest
No potential conflicts of interest were disclosed.
Funding sources
This work was supported by Mount Sinai Children׳s Environmental Health Center (CEHC Pilot Grant Program 0285-7451) and the European Commission׳s Inco-Copernicus Programme (Contract IC15-CT96-0313). In Warsaw, the study was supported by a grant from the Polish State Committee for Scientific Research (Grant SPUB-M-COPERNICUS/P-05/DZ-30/99/2000). Regina Martinez worked on this study under Mount Sinai Undergraduate Research Scholarship.
Acknowledgments
This study would not have been possible without the support of all the study participants and the research staffs from Warsaw, Poland. The authors thank G. Ferro for his expertise regarding data management.
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