We review current knowledge on the trends and drivers of global wildfire activity, advances in the measurement of wildfire smoke exposure, and evidence on the health effects of this exposure. We describe methodological issues in estimating the causal effects of wildfire smoke exposures on health and quantify their importance, emphasizing the role of nonlinear and lagged effects. We conduct a systematic review and meta-analysis of the health effects of wildfire smoke exposure, finding positive impacts on all-cause mortality and respiratory hospitalizations but less consistent evidence on cardiovascular morbidity. We conclude by highlighting priority areas for future research, including leveraging recently developed spatially and temporally resolved wildfire-specific ambient air pollution data to improve estimates of the health effects of wildfire smoke exposure.

There is increasing understanding, globally, that climate change and increased pollution will have a profound and mostly harmful effect on human health. This review brings together international experts to describe both the direct (such as heat waves) and indirect (such as vector‐borne disease incidence) health impacts of climate change. These impacts vary depending on vulnerability (i.e., existing diseases) and the international, economic, political, and environmental context. This unique review also expands on these issues to address a third category of potential longer‐term impacts on global health: famine, population dislocation, and environmental justice and education. This scholarly resource explores these issues fully, linking them to global health in urban and rural settings in developed and developing countries. The review finishes with a practical discussion of action that health professionals around the world in our field can yet take.

Particulate matter (PM) from atmospheric aerosols contains carbons that are harmful for living organisms and the environment. PM can originate from vehicle emissions, wearing of vehicle components, and dust. Size and composition determine PM transport and penetration depth into the respiratory system. Understanding PM emission characteristics is essential for developing strategies to improve air quality. The number of studies on carbon isotope composition (¹³C/¹²C) of PM samples to characterise emission factors has increased. The goal of this review is to integrate and interpret the findings from ¹³C/¹²C carbon isotope ratio (δ¹³C, ‰) analyses for the most common types of emission sources. The review integrates data from 25 studies in 13 countries. The range of δ¹³C of PM from vehicle emissions was from −28.3 to −24.5 ‰ and for non-vehicle anthropogenic emissions from −27.4 to −23.3 ‰. In contrast, PM ranges for δ¹³C from biomass burning sources differed markedly. For C₃ plants, δ¹³C ranged from −34.7 to −25.4 ‰ and for C₄ plants from −22.2 to −13.0 ‰. The ¹³C/¹²C isotope analysis of PM is valuable for understanding the sources of pollutants and distinguishing vehicle emissions from biomass burning. However, additional markers are needed to further distinguish other anthropogenic sources.

Background: Ambient air pollutant (AAP) exposure is associated with adverse pregnancy outcomes, such as preeclampsia, preterm labor, and low birth weight. Previous studies have shown methylation of immune genes associate with exposure to air pollutants in pregnant women, but the cell-mediated response in the context of typical pregnancy cell alterations has not been investigated. Pregnancy causes attenuation in cell-mediated immunity with alterations in the Th1/Th2/Th17/Treg environment, contributing to maternal susceptibility. We recruited women (n = 186) who were 20 weeks pregnant from Fresno, CA, an area with chronically elevated AAP levels. Associations of average pollution concentration estimates for 1 week, 1 month, 3 months, and 6 months prior to blood draw were associated with Th cell subset (Th1, Th2, Th17, and Treg) percentages and methylation of CpG sites (IL4,IL10, IFNγ,andFoxP3). Linear regression models were adjusted for weight, age, season, race, and asthma, using aQvalue as the false-discovery-rate-adjustedp-value across all genes.Results: Short-term and mid-term AAP exposures to fine particulate matter (PM_2.5), nitrogen dioxide (NO₂) carbon monoxide (CO), and polycyclic aromatic hydrocarbons (PAH₄₅₆) were associated with percentages of immune cells. A decrease in Th1 cell percentage was negatively associated with PM_2.5(1 mo/3 mo:Q < 0.05), NO₂(1 mo/3 mo/6 mo:Q < 0.05), and PAH₄₅₆(1 week/1 mo/3 mo:Q < 0.05). Th2 cell percentages were negatively associated with PM_2.5(1 week/1 mo/3 mo/6 mo:Q < 0.06), and NO₂(1 week/1 mo/3 mo/6 mo:Q < 0.06). Th17 cell percentage was negatively associated with NO₂(3 mo/6 mo:Q < 0.01), CO (1 week/1 mo:Q < 0.1), PM_2.5(3 mo/6 mo:Q < 0.05), and PAH₄₅₆(1 mo/3 mo/6 mo:Q < 0.08). Methylation of theIL10gene was positively associated with CO (1 week/1 mo/3 mo:Q < 0.01), NO₂(1 mo/3 mo/6 mo:Q < 0.08), PAH₄₅₆(1 week/1 mo/3 mo:Q < 0.01), and PM_2.5(3 mo:Q = 0.06) whileIL4gene methylation was positively associated with concentrations of CO (1 week/1 mo/3 mo/6 mo:Q < 0.09). Also,IFNγgene methylation was positively associated with CO (1 week/1 mo/3 mo:Q < 0.05) and PAH₄₅₆(1 week/1 mo/3 mo:Q < 0.06).Conclusion: Exposure to several AAPs was negatively associated with T-helper subsets involved in pro-inflammatory and anti-inflammatory responses during pregnancy. Methylation ofIL4, IL10, andIFNγ geneswith pollution exposure confirms previous research. These results offer insights into the detrimental effects of air pollution during pregnancy, the demand for more epigenetic studies, and mitigation strategies to decrease pollution exposure during pregnancy.