Evolution is in the air

Abstract

The Industrial Revolution brought economic growth which enabled higher living standards and improved population health. However, it was driven by increased energy production and consumption which are the primary drivers of environmental damage including air pollution. In the last decade, much of the world has experienced worsening air quality. The health impacts of air pollution have been widely investigated, and potential mechanisms have been proposed. However, these mechanisms do not comprehensively explain how the human species is affected. Given that growth and reproduction are two crucial components in the process of evolution, I undertook an investigation of the association of air pollution with child growth and development and their subsequent impact on later life health informed by an evolutionary perspective.

Based on a large population-representative Hong Kong Chinese birth cohort, “Children of 1997”, I investigated the effects of four air pollutants (particulate matter (PM) with a diameter of 10 micrometres or less (PM10), sulfur dioxide (SO2), nitric oxide, and nitrogen dioxide) in utero, in infancy (age 0-<2 years), and in childhood (age 2-<8 years) simultaneously. Specifically, I investigated the associations of air pollution with birth outcomes (birth weight and gestational age), pubertal development at age ~11 years, and height and adiposity (body mass index (BMI)) at age ~9, ~11, ~13, and ~15 years. I then investigated a potential mechanism by which air pollution may affect bone health, i.e., inflammation. Specifically, I assessed whether inflammation is causally associated with bone mineral density (BMD) using a two-sample Mendelian randomization. Next, I investigated an alternative mechanism that is relevant to disease development, i.e., epigenetics. Specifically, I assessed the mediation by blood deoxyribonucleic acid (DNA) methylation in mid-childhood (median age 7.7 years) for the associations of air pollution in utero and at age 0-<6 years with sex-specific onset of puberty and mid-childhood adiposity with early adolescence cardio-metabolic risk (median age 12.9 years) in Project Viva in the United States. My findings show complex associations of air pollution with growth and development. Trimester-specific associations existed for birth outcomes. Sex-specific associations for pubertal development and BMI were observed. SO2 was associated with transiently shorter height. These findings imply endocrine disrupting effects of air pollution. Genetically predicted inflammatory markers were not associated with lower BMD, suggesting air pollution may affect bone health via alternative mechanisms. DNA methylation may play a role in the associations of higher sulfate with later onset of puberty in girls and of adiposity with cardio-metabolic risk. Taken together, air pollution may exert endocrine disrupting effect and thereby affect child growth and development. The alteration of the trajectory of growth and development may be a response to the environment to improve the chance of reproductive success. The underlying epigenetic mechanisms that facilitate these responses may also be responsible for the undesirable health conditions such as bone loss and higher cardio-metabolic risk in later life. The evolutionary approach in public health may improve our understanding of how extrinsic factors affect health, based on which scientists and policymakers can design effective and efficient interventions.