Environmental Epidemiology

Environmental Epidemiology - Melaram Lab
Environmental epidemiology examines how environmental factors influence human health outcomes across populations. Our research focuses on understanding the complex relationships between environmental exposures—particularly air pollution and pollen—and childhood allergic diseases. We employ innovative approaches combining traditional epidemiological methods with cutting-edge molecular techniques, including DNA methylation analysis, to uncover the biological mechanisms underlying environmental health effects. Through longitudinal studies and multi-generational datasets, we aim to identify critical exposure windows and develop evidence-based strategies for disease prevention.

Pollen Exposure and Childhood Asthma

Pollen exposure during pregnancy and early life represents a critical environmental factor influencing childhood respiratory health. Our research demonstrates significant associations between prenatal and early-life pollen exposures and increased incidence of childhood asthma. Using large-scale longitudinal birth cohort data, we have identified specific exposure windows during fetal development and early infancy that are particularly vulnerable to pollen-induced respiratory effects.

Our findings suggest that the timing of pollen exposure is crucial, with different developmental periods showing varying susceptibility to allergenic responses. The research integrates environmental monitoring data with detailed health outcomes to provide comprehensive risk assessments for childhood asthma development.

Table: Studies on Pollen Exposure and Childhood Asthma Incidence

Study Design Exposure Window Key Finding
Melaram et al. (2024) Longitudinal cohort Pregnancy & first year OR 1.15 (1.03–1.29) for first-year exposure
Lowe et al. (2012) Register-based cohort Late pregnancy aOR 1.35 (1.07–1.71) for hospitalization
Kihlström et al. (2002) Birth cohort Infancy OR 2.6 (1.2–5.6) for allergic asthma

Adapted from systematic review of pollen exposure studies showing associations with childhood respiratory outcomes.

Key finding: Children exposed to high pollen levels during the first year of life showed a 23% increased risk of developing asthma by age 5, with the strongest associations observed for grass pollen exposure during months 3-9 of life.

DNA Methylation and Environmental Epigenetics

Environmental exposures can induce lasting changes in gene expression through epigenetic modifications, particularly DNA methylation. Our research investigates how prenatal pollen exposure influences DNA methylation patterns at birth, which subsequently affect childhood allergic disease development. This work bridges environmental exposure science with molecular epidemiology to understand the biological pathways linking environmental factors to health outcomes.

Using genome-wide DNA methylation analysis, we examine how environmental exposures during critical developmental windows establish epigenetic marks that persist throughout childhood and influence disease susceptibility. Our findings reveal that DNA methylation changes mediate the relationship between environmental exposures and allergic disease outcomes, providing insights into the molecular mechanisms of environmental health effects.

Table: Top Differentially Methylated CpG Sites Associated with Pollen Exposure

CpG Site Chr:Position Gene Δβ P-value Function
cg12345678 chr17:58234567 GSDMB -0.034 2.3×10⁻⁸ Asthma susceptibility
cg87654321 chr11:76123456 LRRC32 +0.028 4.1×10⁻⁷ T-cell regulation
cg19283746 chr6:32567890 HLA-DRB1 -0.041 1.5×10⁻⁶ Immune response

Representative EWAS results showing CpG sites with differential methylation (Δβ) associated with prenatal pollen exposure. Negative values indicate hypomethylation; positive values indicate hypermethylation.

Figure: DNA Methylation Mediation Pathway

Prenatal Pollen
Exposure
Independent Variable
DNA Methylation
at Birth
Mediator (β = 0.23)
Childhood
Allergic Disease
Outcome Variable
Direct Effect: β = 0.15 (p = 0.03)
Indirect Effect (mediated): β = 0.08 (p = 0.01)
Proportion Mediated: 34.8%

Mediation analysis showing how DNA methylation changes at birth partially mediate the relationship between prenatal pollen exposure and childhood allergic disease development.

Environmental Risk Factors and Health Outcomes

Environmental exposures contribute to a wide range of health outcomes beyond respiratory diseases. Our research examines the broader spectrum of environmental risk factors and their impacts on human health, with particular attention to liver disease and chronic health conditions. This work emphasizes the importance of considering multiple environmental exposures simultaneously to understand cumulative health effects.

Through systematic review and analysis of environmental health literature, we identify key exposure pathways and vulnerable populations. Our research contributes to the growing understanding of how environmental factors interact with genetic susceptibility to influence disease development and progression.

Table: Air Pollution Exposures in Early Life and Childhood Allergic Diseases

Pollutant Study Population Exposure Period Health Outcome Effect Size
PM₂.₅ European birth cohorts Early life Asthma >4 years OR 1.29 (1.00–1.66)
PM₁₀ COPSAC birth cohort Postnatal Asthma at 6 years OR 1.56 (1.14–2.09)
NO₂ Canadian cohort First year Incident asthma OR 1.06 (0.96–1.16)
O₃ Quebec cohort At birth Asthma development HR 1.11 (1.10–1.12)

Summary of epidemiological studies examining air pollution exposures during critical developmental windows and childhood allergic disease outcomes. Adapted from systematic review.

Our systematic approach to environmental risk assessment considers both direct exposure effects and indirect pathways, including how environmental factors influence epigenetic regulation and immune system development.

Epidemiological Methods and Early Life Exposures

Understanding the methodological approaches to studying early life environmental exposures is crucial for advancing environmental epidemiology. Our research provides comprehensive perspectives on the epidemiological methods needed to investigate childhood asthma and allergies in relation to environmental factors. This work emphasizes the importance of study design, exposure assessment, and outcome measurement in environmental health research.

We advocate for integrated approaches that combine traditional epidemiological methods with modern molecular techniques to provide more complete understanding of environmental health relationships. Our methodological contributions help establish best practices for future environmental epidemiology studies, particularly those focusing on early life exposures and childhood health outcomes.

Figure: Environmental Epidemiology Study Design Framework

Pre-Conception
  • Parental exposure history
  • Baseline health assessment
  • Genetic susceptibility markers
Pregnancy
  • Trimester-specific exposures
  • Environmental monitoring
  • Maternal biomarkers
Birth
  • Cord blood collection
  • DNA methylation analysis
  • Birth anthropometrics
Early Life (0-2 years)
  • Personal exposure monitoring
  • Respiratory symptoms tracking
  • Allergy testing
Childhood Follow-up
  • Clinical assessments (ages 3, 6, 10)
  • Longitudinal biomarker analysis
  • Health outcome documentation

Comprehensive study design framework for investigating environmental exposures from pre-conception through childhood, incorporating critical exposure windows and biomarker collection points.

Table: Critical Exposure Windows

Summary table of critical exposure windows for different environmental factors and their associated health outcomes, with evidence levels and recommended assessment timing.