UC Berkeley

The environment—defined here as the physical, chemical, biological, and social factors external to a person—has a significant role in the emergence, transmission, and severity of infectious diseases. Further, emerging infectious diseases take on new urgency in the context of climate change, growing populations, and persistent social inequity. In this dissertation, I examine several major environmental determinants of COVID-19 and coccidioidomycosis, estimating their role in structuring patterns of incidence and severity. The recent emergence of SARS-CoV-2 underlines the critical nature of an understanding of the environmental determinants of emerging infectious diseases. Chapter 1 reviews the multiple pathways through which the environment can affect infection with, severity of, and morbidity from COVID-19. I focus on four major categories of exposure: air pollution, chemicals, climate, and the built environment. I build a framework of interlinking mechanisms of action that clarifies upstream and downstream points of intervention and is applicable to other emerging infectious diseases. I summarize the state of epidemiologic and laboratory-based research early in the pandemic, identifying key methodological challenges and opportunities for reductions in adverse environmental impacts on COVID-19 that may yield substantial public health co-benefits. Fine mineral dust is an emerging exposure of concern that is predicted to increase due to escalating climate change, desertification, urbanization, and agricultural output. What is more, emerging evidence suggests that exposure is positively associated with adverse health outcomes including childhood asthma, wheeze, coccidioidomycosis, and mortality. In chapter 2, I estimate the extent to which fine mineral dust exposures are disproportionately distributed across axes of societal advantage and disadvantage as characterized by race, ethnicity, and socioeconomic status. I find that fine mineral dust exposure patterns mirror those of many other criteria air pollutants, with Hispanic/Latinx, Black, and low-income populations exposed to 12.23%, 3.26%, and 6.00% higher concentrations as compared to the total population and high-income populations in California. Disparities persisted across the study period and were particularly pronounced in the southern San Joaquin Valley and Inland regions of the state. Recent decades have seen marked increases in incidence of coccidioidomycosis across California and within new regions of the state. As infection occurs post-inhalation of Coccidioides spp. arthroconidia—often in association with aerosolized soil—understanding the spatiotemporal heterogeneity of risk posed by exposure to fine mineral dust is critical to public health communication and prevention efforts. In chapter 3, I estimate the exposure-response relationship between fine mineral dust concentration and coccidioidomycosis incidence using a distributed lag non-linear framework, as well as variation in risk across time, space, and climatological variables of relevance to the ecology of Coccidioides. I find that exposure to fine mineral dust in the one to three months preceding case onset are strongly associated with coccidioidomycosis incidence, with a cumulative increase in exposure from 0.1 g/m3 to 1.1 g/m3 associated with a 60% increase in coccidioidomycosis incidence. Further, the exposure-response is variable across counties and season of exposure, with exposures occurring in the summer months and San Luis Obispo County and western Madera County particularly strongly associated. Disparities in incidence of coccidioidomycosis across race and ethnicity have persisted across the last two decades and much of California. However, the underlying mechanisms behind this phenomenon are not well understood. Chapter 4 examines the role of adverse environments as mediators of racial and ethnic disparities in infectious diseases. I adapt a longitudinal g-computation framework to estimate the extent to which highly disadvantaged environments experience higher concentrations of fine mineral dust and, accordingly, higher incidence rates of coccidioidomycosis. I find that elevated fine mineral dust concentrations are a modest, though significant, mediator of the relationship between residential segregation and coccidioidomycosis incidence, explaining approximately 6.69% of the association. I conclude by highlighting major findings from each chapter of this dissertation, discussing major open questions, and suggesting future research priorities. Overall, environmental determinants of emerging infectious diseases are critical to both estimate and eliminate, with particular attention needed in areas and communities that have historically been overburdened by intersecting threats. To that end, equitable public health surveillance as well as the expansion of environmental monitoring networks and the provision of preventative health resources will be critical to efforts to minimize the effects of emerging infectious diseases.