Childhood exposure to exhaust linked to insulin resistance at age 24

Insulin resistance is a key precursor to type 2 diabetes and cardiovascular complications. Over the past two decades, it has increasingly been detected in adolescents and young adults. Traditionally, the focus of prevention has been on nutrition, body weight, and physical activity. However, increasing evidence indicates that urban air, especially traffic pollutants (TRAP), independently contribute to the development of metabolic disorders from childhood.

Why emissions and NOx?

Nitrogen oxides (NO and NO₂, collectively NOx) are a characteristic marker of road traffic. They correlate with other exhaust components (ultrafine particles, organic and nitrosating compounds) and are used to assess the proximity to emission sources. Biologically, NOx and associated impurities trigger systemic low-level inflammation and oxidative stress, disrupt the function of the endothelium, mitochondria and adipose tissue, increase liver lipotoxicity and tissue resistance to insulin. Early, intrauterine and childhood exposures coincide with critical windows of development of the metabolic and immune systems, making them potentially particularly vulnerable.

What was already known

• Children living closer to highways or in areas with high TRAP loads are more likely to be overweight and have a higher BMI by school age.
• In adolescence, air pollution was associated with increased HOMA-IR, abnormal lipid profiles and higher HbA1c levels.
• Several studies have shown that the TRAP → diabetes/insulin resistance association is partly mediated by abdominal fat and total body weight—but the exact proportions of mediation and the temporal order have remained unclear.

In a California longitudinal study of 282 people followed from their mothers’ pregnancies to age 24, higher childhood exposure to exhaust oxides of nitrogen (NOx) was associated with increased insulin resistance in adulthood. Almost 42% of this association was mediated by a body weight trajectory: higher BMI at age 13 and faster weight gain thereafter. The study is published in JAMA Network Open.

Why is this important?

• Insulin resistance is the prelude to type 2 diabetes. It is becoming “younger” and is increasingly found in teenagers and young adults.
• Transport pollutants (TRAP: a mixture of gases and particles from vehicle exhausts) are associated with diabetes risks, but whether the risk is mediated through direct effects on metabolism or through weight gain has been unclear.
• The new study is the first to truly separate the time periods: first air pollution (from pregnancy to age 13), then BMI trajectories (13–24 years), and only then metabolic analyses at age 24.

How was it researched?

• Cohort: Meta-Air2 subsample of the renowned Children's Health Study (Southern California). Participants were recruited in kindergarten/first grade and then followed regularly.
• Exposure: for each child, the average concentration of traffic NOx near the home was reconstructed monthly (model CALINE4) from pregnancy to 13 years; in addition, the traffic density within a radius of 300 m was calculated.
• Body weight: objective measurements at 13, 15 and 24 years → from which were constructed:
  • BMI at 13 years (starting point),
  • rate of BMI growth from 13 to 24 years.
• Metabolic results (at 24 years):
  • HOMA-IR (fasting glucose and insulin resistance index),
  • HbA1c (glycated hemoglobin).
• Statistics: Sequential mediator model (PROCESS, model 6) adjusted for age, sex, race/ethnicity, smoking, parental education, family history of diabetes.

Key results (numbers in plain language)

• Each +1 standard deviation in childhood NOx exposure (≈18.7 ppb) is associated with:
  • +0.71 to BMI at 13 years (95% CI: 0.29–1.13),
  • +0.55 to HOMA-IR at 24 years (95% CI: 0.23–0.87).
• Mediation via weight: BMI at age 13 + accelerated BMI growth from age 13 to age 24 explained 41.8% of the total NOx → insulin resistance association (β indirect path 0.23; 95% bootstrap CI 0.01–0.52).
• Similar, albeit more modest, signals were obtained for HbA1c: +0.08 percentage points of HbA1c per 1-SD increase in NOx.
• Comparison of extreme quartiles of NOx exposure in childhood:
  • BMI at 13 years: 21.9 vs. 20.0,
  • BMI at 24 years: 28.4 vs. 25.1,
  • HOMA-IR: 2.8 vs 1.4,
  • HbA1c: 5.5% vs 5.2%.
    Differences remained significant after adjustment.
• In terms of gender, the mediating role of BMI was statistically significant in girls; in boys, the trend was similar, but the power may have been insufficient

What does this mean (and why might it be)

• Childhood exhaust → higher BMI → insulin resistance. Inflammation from inhaling TRAP can change the functioning of adipose tissue and the liver, shift lipid and carbohydrate metabolism, increase visceral fat - all of which worsens the response of cells to insulin.
• At the same time, the direct component (≈58% of the total connection) that does not pass through body mass is also preserved: for example, the effect on mitochondria, endothelium, systemic inflammation.

Restrictions

• Observational design: these are associations, not proven causation.
• The sample size (n=282) limits fine-grained subgroup analysis.
• Cohort: Urban Southern California; generalizability to other regions needs to be confirmed.
• There were not enough intermediate data between 15 and 24 years for a fully sliding mediator model.

Practical conclusions - what can be done now

For families and schools

• If possible, choose routes and time for walks/travel to school away from highways (even +100–200 m significantly reduces TRAP).
• Ventilation - wisely: open windows when traffic is minimal; keep them closed during rush hour, especially on the ground floors near the road.
• Indoor filters (HEPA/carbon): Reduce particles and some gases indoors.
• Regime, nutrition, movement: independent “safety net” — sufficient activity, vegetables/fruits/whole grains, minimum sweetened drinks; regular sleep. These measures reduce the risk of weight gain — and it is through weight that a significant part of the path to insulin resistance passes.

For cities and politics

• Green buffers, noise protection, “life strips” between highways and schools/kindergartens.
• Clean transport (electric/hybrids, public transport, cycling and walking infrastructure) and low emission zones.
• Layout: do not place children's facilities in the first rows to highways.

For doctors and health services

• In high TRAP areas, strengthen weight/metabolism screening in adolescents: monitor BMI trajectories, and implement early behavioral interventions if needed.
• In family conversations, directly discuss the role of the environment: this reduces stigma and increases the effectiveness of assistance.

Conclusions

The work adds an important link to the chain of “exhaust → metabolic risk”: childhood exhaust pushes BMI up as early as age 13, and then accelerated weight gain helps “carry” the risk to insulin resistance in our 20s. So protecting children from traffic pollution and maintaining a healthy body weight are not two competing priorities, but two halves of the same solution.