We may need to consider ambient air pollution exposure in obesity care models.
We all know the causes of overweight and obesity are multifactorial. We also know Australia has one of the highest rates of obesity in the world.
According to the Australian Institute for Health and Welfare, in 2017-2018 67% of Australians aged 18 and over were overweight or obese (36% were overweight but not obese, and 31% were obese), with higher rates now in adult males and the older age groups. There are currently 14 million overweight or obese Australians. In 2017–2018, 25% (1 in 4) children and adolescents aged 2–17 were overweight or obese in Australia; 17% were overweight and 8.2% were obese. The proportion of being overweight and obese in children varied across age groups, but on average were equal for males and females.
But one of those risk factors may come from a surprising source: air pollution.
Air pollution and type 2 diabetes
Ambient air pollution such as particulate matter (PM2.5 and PM10, nitric oxide (NO), nitrogen dioxide (NO2), ozone (O3), and polycyclic aromatic hydrocarbons (PAHS), are now recognised as likely risk factors for the development of type 2 diabetes. The Global Burden of Disease Study 2019 estimated that about a fifth of the global burden of type 2 diabetes is attributable to PM2.5 pollution.
This demonstrates the need to consider and include ambient air pollution exposure assessment within primary health care models and explore new ways to assess its impact and implement air pollution mitigation and preventative interventions to reduce the incidence of obesity and of type 2 diabetes.
A systematic review of high-quality epidemiological studies demonstrated that ambient air pollutant exposure, especially for PM2.5 and PM10 had significant association and prevalence with the incidence of type 2 diabetes, and that diabetic patients may be more vulnerable to air pollutant exposure. The study results found NO2 exposure also raised type 2 diabetes prevalence.
Ambient air pollution incidence and obesity
Epidemiological studies also demonstrate that long-term air pollution exposure may be a contributor to obesity and risk compounding throughout the lifespan with intergenerational and demographic influence.
A recent systematic review and meta-analysis of epidemiological studies indicated that air pollution correlated with childhood obesity and weight gain, and is regarded as a probable risk factor, but long-term, large-scale studies are still required. The research demonstrated that for obesity, the association was considerable with exposure to the much finer particulate matters: PM1 and PM2.5, with a rise in BMI status with 10mcg/m3 increment in exposure to PM10, PM2.5, and NO2.
Learning from retrospective data we can anticipate PM2.5 exposure from wildfires. The Australian 2019-20 bushfires were unprecedented in intensity and spread, with short-term particulate matter exposure experienced in NSW, Queensland, and Victoria, causing substantial health impact. At the time of writing, no evidence of the long-term health impact on weight or prediabetes had been studied. According to the literature there may be in utero effects, including for maternal gestational diabetes.
Biological mechanisms
The literature cites biological mechanisms of outdoor and indoor air pollution with obesity and type 2 diabetes to include vascular insulin resistance and metabolic disturbances caused by inflammation, immune activation, oxidative stress, metabolic dysregulation, intestinal flora disorders and genetic polymorphism, commencing in utero (see: here, here and here).
Animal and cellular studies conclude metabolism-disrupting chemical exposure including toxic pesticides found in air pollution (obesogens) reduce cellular metabolic functioning and may directly contribute to obesity (here and here), with exposure occurring throughout the lifespan and influencing subsequent generations through epigenetic influences.
Intergenerational influence, multigenerational exposure risk and adaptations
Obesity can be a long-term recurring health condition, perpetuated by several risk factors including exposure to outdoor and indoor air pollutants occurring throughout an individual’s life span and accumulating over time. As an individual ages, the ability to remove air pollutants reduces, that may further increase the risk of obesity later in life.
Metabolism-disrupting chemicals found in air pollution change epigenetic patterns and gene expression in utero – increasing susceptibility to metabolic disease in childhood and throughout life (here and here).
The case for a precision-medicine approach
Obesity is a public health crisis, which can originate from metabolic changes commenced in utero and amplified throughout life stages.
Ambient air pollution contributes to changes in metabolic factors and body weight influencing the health of generations. Since the components of air pollution are diverse, mechanisms of action are unique to the individual, indicating the need for a precise, personalised, holistic approach to obesity prevention and management.
Narelle Grant is a PhD candidate and education research and development manager at the Australasian College of Nutritional and Environmental Medicine.
Associate Professor Vicki Kotsirilos AM is a GP with an interest in Environmental Medicine.
