The document discusses opportunities for integrating environmental epidemiology and infectious disease epidemiology. It argues these fields commonly focus on prevention, exogenous disease determinants like pollutants and microbes, and influence public policy. The author proposes a hybrid "environmental infectious disease epidemiology" field with an expanded view of environment and infectious disease determinants. Examples are given of how pollution, climate change, and environmental toxicants like PFAS may increase susceptibility to infection. More research is needed to better understand these relationships and inform public health.

1. Global Environmental Pollution and
Resistance to Infections
David A. Savitz
Brown University School of Public Health

2. Intersection of Environmental and
Infectious Disease Epidemiology
• Both are advanced, productive, but separate
research areas
• Environmental epidemiology
– Focus on exposure assessment, pollutant impact on
disease, mitigation of exposure
• Infectious disease epidemiology
– Focus on determinants of vulnerability, causes of
spread, interventions to reduce infection
• Separate fields for training, in public health
departments, public perceptions, limited joint
activities – opportunity and need to change

3. Commonalities of Environmental and
Infectious Disease Epidemiology
• Focus on prevention
• Concern with the environments in which people
live and work
• Focus on exogenous determinants of disease –
chemicals/physical pollutants, microorganisms
• Uncertainty about magnitude of health impact
and how best to reduce risk
• Prominent role in public policy – intersections
could have large impact on cost/benefit
assessment of policy alternatives

4. Cultivate Hybrid Field: “Environmental
Infectious Disease Epidemiology”
• “Environment” expanded beyond chemical and
physical agents to include built environment,
social environment, and microbial environment
• “Infectious disease” determinants include
environmental pathways (e.g., vector-borne
disease, crowding, water sanitation), parallel to
include environmental toxicants
• Consider established and potential points of
intersection for models

5. Microorganisms as Pollutants
• Agricultural activities raise environmental
concerns
• Longstanding focus on pesticides and fertilizers
• Intensive livestock operations raised concern
with fecal contamination of drinking water
• Cross-species transmission of coronavirus
results from analogous events: agricultural
practices leading to “pollution” of the human
environment
• Consider “exposome” that includes pollutants
and microorganisms

6. Tradeoff of Chemical
and Microbial Pollutants
• Water sanitation has profound public health
benefit
• Microbial threats to drinking water persist
worldwide, require monitoring and treatment
• Water chlorination to control infection generates
disinfection by-products which include known
mutagens and carcinogens
• Finding the optimal balance through engineering
controls based on tradeoff among chemical
contaminants, risk of infection, and cost
• Analogous tradeoffs for pesticides and malaria

7. Climate Change and Distribution of
Infectious Disease
• Many infectious diseases are spatially limited
based on climate and weather, including
extreme weather events such as floods
• Most obvious direct impact of climate change on
human health is expanding the range of tropical
diseases (malaria, Dengue)
• Profound public health impact, motivation for
prevention, opportunity for preparation

8. Environmental Pollution May Reduce
Resistance to Infection
• Plausible biological pathways for chemical
exposures to alter immune response to infection
• Severe immune deficiency markedly raises risk
of acquiring infection, increased severity of
disease
• Chemical pollutants may negatively affect
immune response to infectious agents
• Not likely to be all or none response but subtle,
widespread, depressed response
• Exposure to elevated levels of PFAS impairs
immune response and may increase
susceptibility to infection

9. Epidemiologic Research
on PFAS and Infection
• Series of studies demonstrating impaired
response to selected vaccines in children: higher
levels of PFAS associated with lower antibody
titer in response to vaccine
• Small impact, restricted to children and not
adults
• Impaired response presumed to increase risk of
acquiring infection but not easily demonstrated
• Evidence on PFAS and infectious disease much
less clear than vaccine response

10. “More Research is Needed”…
• Need for improved methods to study
environment, immunologic impairment, and
disease
– Vaccine response and disease risk
– Ability to detect subtle changes in infectious disease
occurrence
• Population models of how impaired immune
response modifies risk in populations
• Apply all available tools for mitigating infectious
disease, possibly including reductions in
environmental pollution