Diabetes

Pollution may increase diabetes risk

‘Children's exposure to traffic pollution could…lead to diabetes' BBC News explains, reporting on a German study.

The study included around 400 children aged 10. Researchers looked at measures of air pollution and proximity to the nearest road at the address each child had lived as a baby.

They also measured each child’s blood sugar and insulin levels.

The second measurement allowed them to calculate each child’s level of insulin resistance – to what extent the cells of the body fail to respond to the hormone insulin (which the body uses to convert blood sugar into energy).

Once insulin resistance reaches a certain level, the symptoms of type 2 diabetes can develop.

The researchers found an association between exposure to air pollution and increased levels of insulin resistance.

However, an association is not the same as proof of a direct causal effect. Living near a busy road would usually imply that a child lives in an urban environment. So there could be a range of environmental factors, other than air pollution, affecting levels of insulin resistance (as well as a wide-range of other possible individual genetic and health-related factors).

The study also does not tell us whether any insulin resistance measured in the child actually had any clinical significance and would lead to a child developing diabetes in later life.

Due to these limitations, further studies in other population samples would be useful.

Where did the story come from?

The study was carried out by researchers from German Center for Diabetes Research and other institutions in Germany, and was funded by German Federal Ministry of Education and Research, and The European Community’s Seventh Framework Programme.

The study was published in the peer-reviewed medical journal Diabetologia.

The quality of the reporting on the study in the UK media is mixed. The BBC News headline gives an accurate representation of the current study as it includes the all-important word ‘may’. However, the Mail Online’s headline linking air pollution to a child’s risk of developing diabetes may be misleading.

This study has many limitations, not least, that increased levels of insulin resistance in childhood, while a risk factor, is not a guarantee that a child will grow up to develop type 2 diabetes.

Also, the association between childhood and diabetes may confuse some readers into thinking that the study was looking at type 1 diabetes – the form of the condition that normally begins in childhood and where the body’s own immune system destroys the insulin-producing cells, so the person is not able to produce any insulin at all.

What kind of research was this?

This was a cohort study looking at whether there was an association between air pollution and insulin resistance.

The researchers say that previous research has shown that traffic and air pollution may increase the risk of diseases affecting the lungs and cardiovascular system.

This is speculated to be due to exposure to pollution that may trigger oxidative stress (a disruption in the body’s ability to repair cellular damage). Pollution could also lead to low levels of inflammation in certain cells of the immune system and those lining the blood vessels.

Animal studies have also suggested that pollution may make cells of the body more resistant to the action of insulin – the hormone released from the pancreas that helps the body to make use of the glucose in the blood.

The researchers say that no study has yet looked at whether traffic-related air pollution can lead to insulin resistance in school-aged children. This German cohort study aimed to look at the relationship between particulate matter in the air and proximity to the nearest road at the child’s birth address, and the child’s insulin resistance when they reached the age of 10.

The limitations of such a study include it being difficult to conclude that the air pollution at the birth address has directly caused the child’s insulin resistance at age 10.

There may be many other genetic, environmental and health-related factors involved.

The study also does not tell us whether any insulin resistance measured in the child has any clinical significance, and whether it is related to later development of type 2 diabetes in adult life.

What did the research involve?

The researchers included sub-groups of 10-year-old children taking part in two separate birth cohorts in Munich, South Germany and Wesel, West Germany:

  • The German Infant Study enrolled almost 6,000 healthy newborns and was a trial looking at the effect of a hypoallergenic infant formulae on a child’s risk of allergy (in addition to looking at other environmental and genetic influences).
  • The Lifestyle-Related Factors study included just over 3,000 healthy newborns and was an observational study looking at the effect of lifestyle factors on the child’s immune system and risk of allergies.

The present study included 397 children randomly sampled from these two cohorts (though 82% came from the Munich cohort) who had blood samples taken for insulin and glucose measurement at age 10, and who had information available for air pollution exposure at the time they were born.

To measure pollution exposure at the birth address, the researchers used models to estimate levels of:

  • nitrogen dioxide (N02)
  • particulate matter of less than 2.5 micrometres in diameter
  • particulate matter of less than 10 micrometres in diameter

Particulate matter is the term for a mixture of solid particles and liquid droplets found in the air.

Measurements were taken at selected monitoring sites on three occasions over 14 consecutive days, and in different seasons.

When conducting their analyses, factors taken into account at each monitoring site were location, surrounding land use, population density and traffic patterns.

Other factors taken into account that could have an influence on the results (confounders) related to the individual child included:

  • parental education (used as an indicator of socioeconomic status)
  • exposure to second-hand smoke
  • height and weight at age 10
  • whether they had started to go through puberty

What were the basic results?

There were no differences between children in the two cohorts, except that those from Wesel were more likely to have been exposed to second-hand smoke and to be of lower socioeconomic status. Pollutant levels were also higher in Wesel than Munich.

After adjustment for all potential study-centre and child-related confounding factors, each two-point standard deviation increase in nitrogen dioxide levels was associated with a 15.8% increase in insulin resistance (95% confidence interval (CI) 3.8 to 29.1).

Each two-point standard deviation increase in particulate matter of less than 10 micrometres in diameter, was associated with a 17.5% increase in insulin resistance (95% CI 1.9 to 35.6). There was no significant association with particulate matter of less than 2.5 micrometres in diameter.

Distance to the nearest road, as would be expected, was significantly associated with pollutant levels (shorter distance equalled higher levels of nitrogen dioxide and particulate matter). Shorter distance to the road was also associated with increased insulin resistance (each 500 metre decrease in distance to road increased insulin resistance by 6.7%, 95% CI 0.3 to 13.5).

The researchers found that the link between pollution levels and insulin resistance was stronger in children who had not moved from their birth address by age 10.

How did the researchers interpret the results?

The researchers conclude that traffic-related air pollution may increase the risk of insulin resistance in children. They say that the associations observed may have important public health implications despite the small effect seen.

Conclusion

This German study looked at the relationship between air pollution and proximity to the nearest road at the child’s birth address, and the child’s insulin resistance when they were aged 10. Though links were found between increasing levels of nitrogen dioxide and levels of particles less than 10 micrometres in diameter and increasing insulin levels at age 10, there are important limitations to bear in mind:

  • Though the researchers have attempted to adjust for many potential confounders, it is difficult to conclude that the air pollution at the birth address has directly caused the child’s insulin resistance at age 10, when there may be many other genetic, environmental and health-related factors involved.
  • The confidence intervals around the increase in insulin resistance with each incremental increase in pollutant levels are very wide. For example, each increase in particles of less than 10 micrometres was associated with a 17.5% increase in insulin resistance, but the actual increase could lie anywhere between 1.9% and 35.6%. This means we can have less confidence in the reliability of these estimates.
  • The study does not tell us whether any insulin resistance measured in the child has any clinical significance, and whether it will be related to higher risk of developing type 2 diabetes in adult life.
  • Also, as mentioned above, the news headlines should not be wrongly interpreted to mean that a child has increased risk of developing type 1 diabetes – the type that readers may associate with start in childhood.  
  • Lastly, the results are based on only a relatively small sample of children from two regions in Germany. Studies of much larger samples from different countries would give more weight to any observations.

Overall, this study cannot prove that air pollution increases a child’s risk of developing diabetes, only that there may be an association with insulin resistance.

As it is unlikely that we are going to live in a world free from air pollution anytime soon, the most effective way of reducing your child’s diabetes risk is to encourage them to take plenty of exercise and eat a healthy diet. These types of good habits in childhood often carry on into adulthood meaning that your child is more likely to maintain a healthy weight – a proven method of reducing type 2 diabetes risk.


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