What’s in Wildfire Smoke?: A Toxicologist Explains the Health Risks and Which Masks Can Help

Smoke is turning the sky hazy across a large swath of the country as dozens of large fires burn, and a lot of people are wondering what’s in the air they’re breathing. As an environmental toxicologist, I study the effects of wildfire smoke and how they differ from other sources of air pollution. We know that breathing wildfire smoke can be harmful. Less clear is what the worsening wildfire landscape will mean for public health in the future, but research is raising red flags

What’s in Wildfire Smoke, and Why is It So Bad for Your Lungs?

If I dare to give the coronavirus credit for anything, I would say it has made people more conscious of the air they breathe. A friend texted me recently after going for a jog in the foothills near Boise, Idaho, writing: “My lungs are burning … explain what’s happening!!!” A wildfire was burning to the east of town – one of hundreds of fires that were sending smoke and ash through communities in hot, dry western states. As an environmental toxicologist, I research how air pollution, particularly wood smoke, impacts human health and disease

Wildfire Smoke Worsens Coronavirus Risk, Putting Firefighters in Extra Danger

As summer approaches, two forces of nature are on a collision course, and wildland firefighters will be caught in the middle. New research suggests that the smoke firefighters breathe on the front lines of wildfires is putting them at greater risk from the new coronavirus, with potentially lethal effects. At the same time, firefighting conditions make precautions such as social distancing and hand-washing difficult, increasing the chance that, once the virus enters a fire camp, it could quickly spread. As an environmental toxicologist, I have spent the last decade expanding our understanding of how wood smoke exposure impacts human health. Much of my current research is focused on protecting the long-term health of wildland firefighters and the communities they serve

Neonatal Lead (Pb) Exposure and DNA Methylation Profiles in Dried Bloodspots

Lead (Pb) exposure remains a major concern in the United States (US) and around the world, even following the removal of Pb from gasoline and other products. Environmental Pb exposures from aging infrastructure and housing stock are of particular concern to pregnant women, children, and other vulnerable populations. Exposures during sensitive periods of development are known to influence epigenetic modifications which are thought to be one mechanism of the Developmental Origins of Health and Disease (DOHaD) paradigm. To gain insights into early life Pb exposure-induced health risks, we leveraged neonatal dried bloodspots in a cohort of children from Michigan, US to examine associations between blood Pb levels and concomitant DNA methylation profiles (n = 96). DNA methylation analysis was conducted via the Infinium MethylationEPIC array and Pb levels were assessed via high resolution inductively coupled plasma mass spectrometry (HR-ICP-MS). While at-birth Pb exposure levels were relatively low (average 0.78 µg/dL, maximum of 5.27 ug/dL), we identified associations between DNA methylation and Pb at 33 CpG sites, with the majority (82%) exhibiting reduced methylation with increasing Pb exposure (q \u3c 0.2). Biological pathways related to development and neurological function were enriched amongst top differentially methylated genes by p-value. In addition to increases/decreases in methylation, we also demonstrate that Pb exposure is related to increased variability in DNA methylation at 16 CpG sites. More work is needed to assess the accuracy and precision of metals assessment using bloodspots, but this study highlights the utility of this unique resource to enhance environmental epigenetics research around the world

Is Adiposity Related to Repeat Measures of Blood Leukocyte DNA Methylation Across Childhood and Adolescence?

Epigenetic modifications such as DNA methylation may influence gene expression and phenotypes, including obesity in childhood. The directionality of this relationship is nevertheless unclear, and some evidence suggests that adiposity modifies the epigenome, rather than the other way around. In this pilot study, we utilize data from the Early Life Exposures in Mexico to Environmental Toxicants (ELEMENT) study to examine whether measures of adiposity in childhood and early adolescence are associated with repeated measures of blood leukocyte DNA methylation at LINE-1 repetitive elements and two genes implicated in growth and adiposity: H19 and HSD11B2. Longitudinal epigenetic data were generated from cord blood and blood from follow-up visits in early and late adolescence. We assessed interactions between age and measures of body mass index (BMI) at 5 years of age and weight, BMI and waist circumference in early adolescence to infer whether adiposity deflects age-related DNA methylation changes throughout childhood. Applying linear mixed-effects models, we found an inverse association between measures of childhood BMI (kg/m2) and early-teen weight (kg) with repeat measures of H19 DNA methylation. We did not observe any statistically significant associations (p-value \u3c .05) between any anthropometric measures and DNA methylation at LINE-1 or HSD11B2. We did not demonstrate statistically significant evidence in support of deflection of age-related DNA methylation trajectories by adiposity-related measures (age by adiposity interaction term). Given the pilot nature of this study, the relationships between repeat measures of DNA methylation and adiposity-measures across childhood merit further exploration in larger study populations

DNA Methylation in Humans and Dogs: Evaluating the Impact of Nutritional and Particulate Exposures

Asthma is among the most common chronic diseases in children, among the leading causes of hospitalization for children, and one of the leading causes of school absenteeism. Discovery of preventable factors and the underlying mechanisms that exacerbate asthma among prevalent cases is important for mitigating the health burden of this childhood disease. Environmental factors such as exposure to particulate matter (PM) or nutritional deficiencies can lead to poor respiratory health among susceptible children. Recent animal studies suggest that PM exposures and dietary nutrients may influence asthma pathways through epigenetic mechanisms. Epigenetic modifications are heritable changes that can regulate gene activity without altering the primary DNA sequence. With respect to allergic or asthma phenotypes, several cytokine and transcriptional factors relevant to the allergy/asthma response pathway and its counter regulation have been shown to be modulated by epigenetic processes. The results of the following research aims may help to elucidate the relationship between PM and dietary exposures, epigenetic responses, and respiratory health outcomes among asthmatic children

Influence of Woodsmoke Exposure on Molecular Mechanisms Underlying Alzheimer’s Disease: Existing Literature and Gaps in Our Understanding

Woodsmoke poses a significant health risk as a growing component of ambient air pollution in the United States. While there is a long history of association between woodsmoke exposure and diseases of the respiratory, circulatory, and cardiovascular systems, recent evidence has linked woodsmoke exposure to cognitive dysfunction, including Alzheimer’s disease dementia. Alzheimer’s disease is a progressive neurodegenerative disorder with largely idiopathic origins and no known cure. Here, we explore the growing body of literature which relates woodsmoke-generated and ambient air pollution particulate matter exposure to Alzheimer’s disease (AD) onset or exacerbation, in the context of an inflammation-centric view of AD. Epigenetic modifications, specifically changes in DNA methylation patterns, are well documented following woodsmoke exposure and have been shown to influence disease-favoring inflammatory cascades, induce oxidative stress, and modulate the immune response in vitro, in vivo, and in humans following exposure to air pollution. Though the current status of the literature does not allow us to draw definitive conclusions linking these events, this review highlights the need for additional work to fill gaps in our understanding of the directionality, causality, and susceptibility throughout the life course

Breathing Wildfire Smoke Can Affect the Brain and Sperm, as Well as the Lungs

Wildfires burning in the western U.S. are sending smoke into communities far from the fires themselves, creating hazardous air for days or weeks at a time. A lot of people are wondering: What does breathing all that smoke do to our bodies? Wildfire smoke is a mix of chemicals and tiny particles that are small enough to evade the body’s defenses and directly affect the lungs. But the damage may not stop there. As environmental toxicologists, we have been investigating the health effects of wildfire smoke on humans, including on parts of the body that you might not expect: sperm and the brain

An Epigenetic Pilot Study Investigating Biomarkers in Maternal-Infant Pairs

Rationale: Particulate matter (PM) is a measurable component of air pollution that has been associated with adverse cardiovascular and respiratory outcomes. Research indicates environmental factors such as air pollution are involved in changes through epigenetic mechanisms during development that may persist into adulthood and even span multiple generations of inheritance. Epigenetics is the study of heritable changes of gene expression that do not alter the actual DNA sequence. One epigenetic mechanism is DNA methylation. Long Interspersed Nuclear Element (LINE-1) is a DNA repetitive element that can be used as a proxy measurement of DNA global methylation. The purpose of this pilot study was to compare epigenetic biomarkers across different sample matrices (i.e. blood and buccal) and across related subjects (i.e. maternal and infant). Methods: Informed consent was provided by pregnant women (n=23) who were recruited through Women, Infants, and Children (WIC), hospital birthing classes, or flyers in obstetrician’s offices. Demographic and medical data was collected from hospital records for both mothers and newborns after birth. Follow-up health surveys were administered by telephone that were designed to collect indicators of pre-asthmatic respiratory symptoms or conditions. Biological samples were collected before or shortly after time of birth at Community Medical Center of Missoula, MT. The samples collected were maternal blood (n=15), umbilical cord blood (n=15), and maternal (n=23) and newborn (n=23) buccal (cheek) cells. Buccal cells were collected and processed according to the Gentra Puregene Kit (Qiagen, Germantown, MD). These biologically accessible tissues serve as surrogates to study gene methylation associated with respiratory health. Samples were stored at -80°C until DNA extraction and subsequent bisulfite treatment. The samples were amplified in duplicates with polymerase chain reaction (PCR). LINE-1 methylation was analyzed with pyrosequencing on a Pyromark Q96 MD (Qiagen, Germantown, MD). All statistical analysis was performed in Statistical Analysis Software (SAS, version 9.3). Results: The mean (standard deviation (sd)) of LINE-1 methylation percentage for mother and infant buccal cell derived DNA were 58.75 (3.89) and 57.16 (2.54), respectively. Percent methylation maximum for mother and infant buccal samples were 70.22 and 64.25, respectively, and minimum were 54.86 and 52.94, respectively. Paired t-test indicated that LINE-1 methylation percentages in maternal buccal samples were higher than methylation percentages in the paired infant samples (mean difference (95%CL) = 4.4 (2.3, 6.6)). The mean (sd) of LINE-1 methylation percentage for mother and infant/cord blood derived DNA were 75.19 (3.17) and 75.86 (3.05), respectively. Percent methylation maximum for mother and infant blood samples were 79.42 and 79.50, respectively, and minimum were 70.39 and 69.31, respectively. Paired t-test indicated that LINE-1 methylation percentages in maternal blood samples were similar to methylation percentages in infant blood samples (mean difference (95% CL) = 0.66 (-2.0,3.3)). Conclusions: LINE-1 methylation percentages between sample matrices (i.e. blood and buccal) and subjects (i.e. maternal and infant) were not correlated. The percent methylation of LINE-1 in DNA from blood was consistently greater than for DNA from buccal tissue for both mother and newborn samples. It was expected that LINE-1 measurements for blood DNA would differ from buccal DNA because circulating blood represents a more diverse cell population. Gene-specific methylation of the promoter region for interferon-γ, a cytokine associated with asthma, will be studied with the remaining samples of bisulfite-treated DNA from this study. Epigenetic changes may serve as useful biomarkers for predicting asthma risk in children exposed to biomass smoke. These methods can be applied to future studies to investigate the epigenetic relationship of prenatal asthma risk and PM wood smoke exposure

Household reporting of childhood respiratory health and air pollution in rural Alaska Native communities

Background. Air pollution is an important contributor to respiratory disease in children. Objective. To examine associations between household reporting of childhood respiratory conditions and household characteristics related to air pollution in Alaska Native communities. Design. In-home surveys were administered in 2 rural regions of Alaska. The 12-month prevalence of respiratory conditions was summarized by region and age. Odds ratios (ORs) were calculated to describe associations between respiratory health and household and air quality characteristics. Results. Household-reported respiratory health data were collected for 561 children in 328 households. In 1 region, 33.6% of children aged/or bronchitis. Children with these conditions were 2 times more likely to live in a wood-heated home, but these findings were imprecise. Resident concern with mould was associated with elevated prevalence of respiratory infections in children (ORs 1.6–2.5), while reported wheezing was associated with 1 or more smokers living in the household. Reported asthma in 1 region (7.6%) was lower than national prevalence estimates. Conclusions. Findings suggest that there may be preventable exposures, including wood smoke and mould that affect childhood respiratory disease in these rural areas. Additional research is needed to quantify particulate matter 2.5 microns in aerodynamic diameter or less and mould exposures in these communities, and to objectively evaluate childhood respiratory health